Grey Matters VC Issue 6

FEATURING Love on the Brain: The Science of Lust, Attraction, and Attachment Hypoxic Conditioning: When Less (Oxygen) is More A Wrinkle in the Mind: How Prions Infect the Brain

SPRING 2023

@greymattersjournalvc GREY MATTERS JOURNAL AT VASSAR COLLEGE | ISSUE 6greymattersjournalvc.org

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GREY MATTERS JOURNAL AT VASSAR COLLEGE | ISSUE 6

TABLE OF CONTENTS 6

LIVING ON THE EDGE: THE SCIENCE BEHIND THRILL SEEKING BEHAVIORS

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by Niah Dang/ art by Max Brenneman

FEATURED ARTICLE

10 LOVE ON THE BRAIN: THE SCIENCE OF LUST, ATTRACTION, AND ATTACHMENT

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BEYOND BABY BLUES: UNPACKING POSTPARTUM DEPRESSION

by Jack Matter/ art by Laurel Obermueller

by Elsie McKendry/ art by Abigail Schoenecker

THE BRAIN-COMPUTER DEBATE: IS THE HUMAN BRAIN LIKE A COMPUTER?

A GLITCH IN THE MATRIX: EXPLORING THE ILLUSION OF DÉJÀ VU

by Dominic Matos and Tamar Paserman/ art by Ming Na

FEATURED ARTICLE

38 A WRINKLE IN THE MIND: HOW PRIONS INFECT THE BRAIN

by Daniella Lorman/ art by Ava Sclafani

by Sufana Noorwez art by Iris Li

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GRIEVING A CHANGING ENVIRONMENT: EXPLORING THE EFFECTS OF CLIMATE CHANGE ON THE PSYCHE

by Jaclyn Narleski/ art by Arden Spehar

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EXPLORING THE POSSIBILITIES OF LIFE WITHOUT A BRAIN

by Sloane Boukobza/ art by Michelle Shaffer

FEATURED ARTICLE

22 HYPOXIC CONDITIONING: WHEN LESS (OXYGEN) IS MORE

by Alex Roth/ art by Anna Bishop

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ISSUE NOTES ON THE COVER

LEARN MORE

Art by Ava Sclafani

Check out our website to read our blog, find out how to get involved, and more at greymattersjournalvc.org.

LET US KNOW If you have any questions or comments regarding this Issue 6, please write a letter to the editor at brainstorm.vassar@gmail.com.

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PRODUCTION STAFF

LUCAS ANGLES Editor-in-Chief

Senior Managing Editor

LUCY VOLINO

OLIVIA GOTSCH

NANAKO KUROSU

ANJALI KRISHNA

JULIA VITALE

AMBER HUANG

AINSLEY SMITH

YUCHEN WANG

CHERRIE CHANG

Senior Editor, Lay Review

Art Executive & Treasurer

ANSHUMAN DAS

Production Manager

Senior Editor, Lay Review

Art Executive

SHAWN BABITSKY

Outreach Coordinator

Senior Editor, General Editing

Senior Editor, Scientific Review

JULIÁN AGUILAR

Layout Executive & Graphic Designer

TALIA MAYERSON Graduate Student Executive

Senior Editor, General Editing

Senior Editor, Scientific Review

MAX FREEDMAN

Website Executive & Graphic Designer

CLEM DOUCETTE Graduate Student Executive

GREY MATTERS JOURNAL AT VASSAR COLLEGE | ISSUE 6

DANIELLA LORMAN Graduate Student Executive

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ARTISTS

AUTHORS

Abigail Schoenecker Anna Bishop Arden Spehar Ava Sclafani Iris Li Laurel Obermueller Max Brenneman Michelle Schaffer Ming Ni

Alex Roth Daniella Lorman Dominic Matos Elsie McKendry Jack Matter Jaclyn Narleski Niah Dang Sloane Boukobza Sufana Noorwez Tamar Paserman

SCIENTIFIC REVIEW

LAY REVIEW

GENERAL EDITING

Alexis Earp Alyssa Gu Caitlin Shi Eve Andersen Frank Ryan Isabel McGuire Lilah Lichtman Maria Cusick Shawn Babitsky

Anna Terry Arden Spehar Chloe Lucas Claire Bennett Emma San Filippo Frederica von Siemens Isabella Sagman James Hatch Jaya Moorjani Jolie Walker Kaitlin Raskin Kenza Squali-Houssaini Laurel Obermueller Martine Schwan Nehal Ajmal Nico Silverman-Lloyd Susanna Osborne Zayn Cheema Zilan Ding

Alex Kaye Avery Bauman Dhriti Seth Dimple Kangriwala Evelynn Bagade Hailey Brigger Hannah Koolpe Jade Hsin Jadon-Sean Sobejana Jas Kaur Jess Camacho Jordan Klembczyk Jordan Norman Liv Lord Maia Beaudry Ninamma Rai Rileigh Chinn Talia Roman Victoria Tager-Geffner

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EDITOR’S NOTE As we proudly unveil the sixth issue of Grey Matters at Vassar College, I am filled with a deep sense of gratitude and accomplishment. This semester marks the end of my tenure as Editor-in-Chief, and I find myself reflecting on the remarkable journey we have undertaken alongside our dedicated general body and outstanding executive board. I am truly grateful for the opportunity to collaborate with such gifted individuals who are united by a passion for making scientific concepts accessible to a broader audience.

Throughout my time at Grey Matters Journal, I have had the honor of not only bringing our readers closer to the science I cherish, but also nurturing the growth and development of future researchers, educators, and medical professionals. Each semester, it has been a privilege to witness the impressive progress our editors and authors make in a matter of weeks. Our authors are able to master both their communication and prose, while our editors are able to deepen their understanding of novel science. All remain committed to the goals of Grey Matters: to explore and liaise with what was previously unknown. By fostering a new movement of accessible science, I am confident that have expanded previously inaccessible knowledgebases to many. As we continue to extend our influence to other Institutions of Higher Learning, I am excited by the impact we will have on many others.

In this issue, you will discover a range of captivating articles, meticulously crafted to ensure a thorough understanding of the science they encompass. Delve into the depths of your emotions for that special someone in “Love on the Brain: The Science of Lust, Attraction, and Attachment,” inhale a potential new treatment for Alzheimer’s Disease in “Hypoxic Conditioning: When Less (Oxygen) is More,” or investigate a perplexing brain disease in “A Wrinkle in the Mind: How Prions Infect the Brain.” We hope that these pieces ignite your curiosity and inspire a profound appreciation for the immense and complex world of brain science.

As we embark on the next chapter of Grey Matters Journal, I am delighted to introduce our incoming executive board members. They are all exceptionally talented in their respective fields and show unwavering commitment to advancing the organization. I am confident that Shawn Babitsky, the incoming Editor-in-Chief, will steer Grey Matters Journal to unprecedented heights under his leadership. I eagerly await reading every article our publication continues to create with the same zeal that has accompanied me for the past three years.

As I bid adieu to my position as Editor-in-Chief, I invite you to join me on an expedition through the human brain and beyond. The future of Grey Matters Journal is bright, and I am honored to have been a part of its journey thus far.

With warmest regards,

Lucas Angles Editor-in-Chief

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LIVING ON THE EDGE

LIVING ON THE EDGE: THE SCIENCE BEHIND THRILL SEEKING BEHAVIORS

by Niah Dang/ art by Max Brenneman a young man rock climbing, thousands of Pthaticture feet in the air. As you take a closer look, you realize he lacks any safety equipment or ropes tethering

him to the wall. There is no harness to catch him if he falls — and it’s a long way down. “What an idiot,” you mutter to yourself, shaking your head. It’s hard to imagine why someone would risk their life like that, seemingly for no reason. And yet, participation in death-defying pursuits has only increased over time [1]. Due to the growing commercialization and accessibility of these risky activities, the general uptick in involvement is unsurprising. Perhaps children watching the X Games and other widely broadcasted representations of extreme sports were exposed early to the world of extreme sports, paving the way for their own future pursuits [2]. These so-called ‘adrenaline junkies’ — who regularly seek out situations that may endanger their lives in search of a thrill — have expanded their endeavors to include an ever-growing number of dangerous activities [3]. ‘Adrenaline junkies’ may choose to walk on the wings of planes midair, scale the rocky sides of active volcanoes, or climb thousands of feet onto jagged rock faces with no backup. There is no clear scientific phenomenon underpinning what tempts people to flirt with death on a daily basis. However, we may begin to understand what drives this thrill-seeking behavior through biological, psychological, and social approaches.

REAPING THE REWARDS: THE ROLE OF DOPAMINE Suddenly emerging into view, a person dressed only in a swimsuit jumps off a cliff and plunges into the murky depths of the ocean below. They break through the water’s surface moments later, gasping for air and dizzy with elation. This activity involves taking a major risk: a slight miscalculation of the jump could result in injury or death [4]. The thrill experienced from this kind of risk is a product of both adrenaline and dopamine, chemical messengers that can have numerous effects on our biological state. As a hor-

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mone, adrenaline travels through the bloodstream to many parts of the body [5]. Dopamine, on the other hand, is a neurotransmitter, so it acts within the brain and nervous system [6, 7]. Hormones and neurotransmitters can change the way our bodies function normally [8, 9]. Think about the twinge of fear masked by

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LIVING ON THE EDGE excitement as you peer over the edge of the diving board. Before you jump, you feel your heart racing, and your breathing becomes shallow. Once you resurface, a rush of satisfaction hits, tempting you to climb back up for another go. Cliff jumpers commonly experience these feelings. This complicated biological phenomenon arises from a combination of the adrenaline response and dopamine reward system [3].

Some neurons work as a part of our body’s limbic system, a collection of brain structures regulated by dopamine [10]. Changes in the amount of dopamine in a pathway commonly called the reward system, can modify behavioral responses to variations in your surroundings [9]. As the name suggests, the reward system elicits and reinforces behaviors associated with rewards, such as finding food. Why would dopamine be released when someone participates in a dangerous activity if it could potentially cause them serious harm? Dopamine is typically released slowly and irregularly, yet can be induced to release in bursts in certain situations [11]. In addition to being released in response to rewarding stimuli, dopamine can also be released during intense or novel experiences. Sudden bursts of dopamine can even encode distinct messages to the body [12]. When someone goes mountain climbing, for instance, they subject their body to dramatically increased physical stress. When augmented by the novelty of a new experience, like an unexplored climbing route, stress leads to an increase in dopamine [13]. Stress, often augmented by the novelty of an unfamiliar scenario, increases dopamine release and strengthens reward-related connections in the brain [9].

for adrenaline, at which we perform our best. When this ‘threshold’ is exceeded, however, it can result in less-than-optimal performance; the perfect balance of adrenaline is vital for success. As a snowboarder skillfully weaves through the trees down the mountain, the physical stress of this activity stimulates adrenaline release and heightens their focus [18]. In fact, when describing the threatening situations that risk-takers subject themselves to, the word ‘rush’ is often used [19]. A rush refers to the feelings of thrill and flow, and thrill is explained by one’s adrenaline levels. Flow is a more nuanced sensation and involves the mental aspect of these extreme activities, specifically when mental focus and physical practice coincide [19]. This rush can provide an extra boost of cognitive and physical energy, making these activities more enticing. Arguably, individuals who engage in extreme activities are thought to be attracted to the rush associated with their activity rather than the intrinsic danger of participation [19].

WORTH THE RISK: THE ROLE OF ADRENALINE When someone is faced with a stressful situation, their body’s fight or flight system kicks in [14].

During this response, the nervous system stimulates the secretion of adrenaline to help prepare the body to react [15]. When a snowboarder glides along the tip of a mountain, they feel the sharp pounding of their heart and their breath begins to quicken [8].

These physical changes are telltale signs that one’s fight or flight response is in full effect. Emotional stress, in particular, has been shown to increase the amount of adrenaline the body produces [17].

Adrenaline elevates oxygen levels in the body, which can increase mental clarity [16]. Emotional stress can also enhance physical performance to a certain extent [17]. We all have our own personal ‘threshold’

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LIVING ON THE EDGE

LOSING YOUR GRIP: WHEN THRILL SEEKING GOES AWRY Adrenaline and dopamine may also be involved in the addictive aspect of chasing adrenaline. In fact, ‘adrenaline junkies’ can experience behaviors similar to someone addicted to drugs or alcohol, especially in their ability to maintain self-control [20].

In the addiction circuitry that underscores drug or alcohol dependence, dopamine and adrenaline are critical in increasing addictive behaviors by causing dysfunction within pathways that control attention and impulse control [4]. Behavioral addictions can be severely threatening to one’s health [21]. Since it is difficult to differentiate between normal and excessive participation in risky activities, behavioral addictions are also harder to classify than substance addictions [21]. However, there are factors that commonly indicate a behavioral dependency, including a lack of control, continued engagement in an activity despite known adverse consequences, and persistent urges to par-

ticipate in a behavior [21]. For instance, Dean Potter, a competitive, well-recognized figure for dangerous extreme sports, engaged in high-lining, wingsuiting, BASE jumping, and other risky sports [4]. Potter also had a history of impulsive behavior — notably, illegally climbing in national parks — that caused him to lose substantial sponsorship deals. Potter was “fiercely competitive and proud… he was prepared to go to extreme lengths to protect and extend his records and accomplishments.” The desire to extend and protect his legacy ultimately cost him his life after unsuccessfully attempting a risky, illegal, and never-before-performed BASE flight at Yosemite National Park [4]. This tragedy exemplifies the true danger behavioral addictions pose and why it is important to continue searching for the reason people return to danger.

IF YOU JUMP, I WILL… Being surrounded by peers activates the systems responsible for social and emotional processing, and can increase the influence of peer pressure [22]. In an effort to be noticed by their peers, some people turn to risky behaviors [22]. Although it may be an annoying question for many teens, parents have a good reason for asking, “If all your friends jumped off a cliff, would you?” Consider a scenario in which all your friends jump from a plane, skydiving down to Earth. Whether we admit it or not, cheers from our friends might push us to jump, and soon, we might be free-falling. Social pressure from our peers is at play with such extreme activities [23]. Throughout our evolutionary history and to this day, humans have been driven to achieve higher status among their peers to obtain power and admiration [24]. Historically, respect from community members has provided survival and reproductive benefits through increased social influence within a group [24]. Status can be achieved in several ways, and risk-taking is one of them [24].

Social groups often reward successful risk-takers with prestige and recognition, outweighing the physical risks of the behavior [25]. Imagine a group of rock climbers constantly pushing each other to new heights. To keep up with the group, members may attempt climbs they would have otherwise deemed too risky to complete alone. This social acceptance, in combination with the biological dopamine reward, can make dangerous behaviors seem well worth the risk. These risky acts even have the potential to facilitate friendships [3]. In groups where members take on extreme activities together, members often come to depend on one another; dangerous elements foster trust and friendship between people [3].

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LIVING ON THE EDGE Daredevil rock climbers may even feel safe enough to try riskier climbs, knowing their companions will catch them if they fall. This social element of encouragement, combined with the perceived safety of having others around, can push group members to explore new heights and surpass their own expectations of their abilities. These friendships can act as a reward loop, motivating people to continue to engage in risky behaviors [3].

HOW SAFE IS TOO SAFE? In our modern society, safety features adorn every corner of our world. Fire alarms alert us when smoke is detected, railings are built so people don’t topple from great heights, and regulations on buildings are enforced to ensure structural soundness.

A prevailing theory as to why the number of people who pursue extreme activities has been increasing over time is known as compensation theory [4, 25,

26]. This theory suggests that in an increasingly modernized world, people feel restricted by the endless safety features of society and compensate for this by partaking in risky activities [4, 25]. This tendency potentially originates from the ‘raw’ human desire for excitement, which precedes modern civilization [25].

We often seek large doses of whatever we feel has been withheld. Maybe bungee jumping into a canyon isn’t a death wish but rather a natural desire for excitement in an overly cautious society.

CHASING THE HIGH: SOME JUST CAN’T GET ENOUGH Why people choose to participate in life-threatening activities is a subject that requires much more research. Several factors contribute to people’s participation in thrill-seeking endeavors. Trying to understand these behaviors through a single perspective would discount the complex interplay of factors that draw people to them. For a young teenage boy, jumping off the roof into the pool below might be his best bet at catching his buddies’ attention and praise. For the tired mom, drained by the same repetitive daily schedule, rock climbing trips with adventurous friends might give her the energy to keep going. For most that participate, it’s the feeling only attainable when you cheat death — a feeling many of us will rarely experience [19]. So, next time you see that young man rock climbing high above the ground, you may shake your head in disapproval and disbelief, but perhaps you will also understand the factors that compel him to stare death straight in the eyes.

References on page 48.

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LOVE ON THE BRAIN

LOVE ON THE BRAIN: THE SCIENCE OF LUST, ATTRACTION, AND ATTACHMENT

by Elsie McKendry/ art by Abigail Schoenecker

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LOVE ON THE BRAIN Thus with a kiss I die,” proclaimed Romeo, “Juliet, standing over Juliet’s still body. In Romeo and playwright William Shakespeare writes of a love so powerful that it drives a man to suicide.

Similar testaments to the power of love can be found across time and cultures, in poetry, music and the tradition of marriage itself. In many ways, love is inexplicable, rendering attempts to define it difficult. ‘Love’ is commonly used as a general term to encapsulate everything ranging from sexual attraction and crushes to deep romantic love. While feelings of lust, attraction, and attachment are often experienced simultaneously, they can exist separately as well. For instance, the love shared between a parent and child demonstrates the separation of attachment from attraction and lust. Alternatively, you may be in love with a long-term partner while still feeling attraction to another person or celebrity crush. Studying the complex distinctions between lust, attraction, and attachment from a neuroscience perspective can help explain why love makes humans feel and act the way we do.

LUST: I CAN’T TAKE MY EYES OFF OF YOU Two college students, Rohan and Charlotte, are at a party. As Rohan watches Charlotte dancing across the room, he wants to be close to her and wanders over to join. While dancing with Charlotte, Rohan notices his growing excitement manifested by her touch and can’t stop thinking about kissing her. He begins to lose self-awareness and feels tempted to act on his impulses. Rohan is enveloped by feelings of lust, a state of sexual arousal characterized by physiological responses that encourage physical intimacy and reproduction [1]. In this moment, Rohan’s passionate reaction can be understood in part by looking at the brain.

pothalamus is a part of the brain that regulates key bodily functions, such as the regulation of sexual drives [4]. Feelings of sexual arousal are elicited when the hypothalamus signals the reproductive system to release sex hormones called testosterone and estrogen [5]. These hormones increase sex drive which in turn helps facilitate genital lubrication and increased genital sensory perception [5, 6]. High levels of estrogen and testosterone also promote the release of dopamine, a chemical messenger active in the brain’s reward system that is crucial for the perception of pleasure in romantic and sexual contexts [16]. These functions make Charlotte and Rohan more receptive to and stimulated by sexual activity. Since sexual arousal is pleasurable, Rohan and Charlotte feel motivated to later return to this physiological state.

Other than hormone production, the inhibition of activity within the prefrontal cortex facilitates sexual activity [2]. Periods of high sexual arousal are associated with suppression of activity in the prefrontal cortex, the portion of the brain responsible for decision making [7]. A lack of prefrontal cortex activity is associated with behaviors such as getting caught up in the moment, the dissolution of usual physical boundaries, and a loss of control [2]. For this reason, Rohan and Charlotte may lose self-awareness and act on impulse, rather than thinking about the potential outcomes of their actions.

Lust is controlled by multiple changes in the brain, including reduced activity in the prefrontal cortex and increased hormone production triggered by the hypothalamus [2]. The prefrontal cortex mediates complex cognitive behaviors, especially those concerning the ability to suppress urges that may lead to socially unacceptable behaviors [2, 3]. The hy-

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LOVE ON THE BRAIN

ATTRACTION: I WANT TO HOLD YOU A week after meeting at the party, Rohan and Charlotte decide to visit an amusement park together.

As Charlotte and Rohan walk through the crowds, Charlotte feels jittery with excitement. Her heart beats quickly, and her palms start to sweat; these symptoms are characteristic of the ‘fight or flight’ response, caused by the sympathetic nervous system, which mediates bodily functions through a network of nerves that are ‘excited’ by being in close proximity to one’s crush. [8]. Attraction, otherwise known as passionate love, refers to the feelings of intense infatuation often present during the formation of relationships, and is known to trigger the sympathetic nervous system [8]. Although love isn’t usually a source of danger, it leads to an arousal state that parallels the physiological effects of fear and excitement. Conversely, these danger responses may also prompt feelings of attraction. In situations where acute stress is external and unrelated to attraction, like when about to ride a rollercoaster, the activation of a person’s fight or flight response may cause the misinterpretation of fear-based arousal as attraction [9, 10]. Therefore, during their second date, Charlotte may find Rohan more attractive than she would have otherwise because she misinterprets her amusement park-induced state as romantic attraction [10]. While extreme stress inhibits attraction, stress in small doses can actually enhance

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it [9]. Activation of the sympathetic nervous system can cause short-term increases in testosterone, thus increasing sexual desire [5, 11]. Emotional connections can also be enhanced by the release of cortisol, a primary stress hormone associated with the formation of social attachment [12].

In addition to physiological arousal, compulsive thinking and intense desire for proximity to another person are characteristics of attraction [13]. In the days following their date, Charlotte replays her experience with Rohan over and over in her mind. She finds herself distracted in class and unable to sleep, obsessively thinking about the next time she will see Rohan.

Dopamine, one of the chemical messengers involved in lust, is partially responsible for Charlotte’s obsessive reaction [14]. Dopamine plays a significant role in the brain’s reward center and reinforces sex-related stimuli by rewarding a person with a ‘high’ when they are interacting with their crush [13]. Charlotte may even begin to feel ‘lovesick,’ as elevated levels of dopamine are associated with feelings of ecstasy, increased energy, sleeplessness, reduced appetite, and anxiety [13]. Moreover, these chemical changes in the brain lead to focused attention on a person, their positive traits, past memories with them, and the sense that they are unique [1].

ATTACHMENT: NOW THAT I’VE FOUND YOU, STAY After a year of dating, Rohan and Charlotte’s relationship has evolved. The anxious butterflies Rohan feels in Charlotte’s presence are replaced by a sense of security. As the boundaries between them dissolve, they can be vulnerable with each other without fear of judgment. This stable and secure state is also referred to as attachment and is characteristic of longterm relationships, marriage, committed friendships, and parent-child relationships [16, 17]. Attachment includes the same desire for proximity and physical contact present in attraction, but it is generally perceived as less urgent [16].

This transition from attraction to attachment is sometimes interpreted as the end of the ‘honeymoon phase’ [18].

As Rohan and Charlotte lay in bed cuddling at night, the release of oxytocin in their bodies contributes to the sense of calmness they feel. Oxytocin is a hormone associated with positive social behavior such as pair bonding, sexual

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LOVE ON THE BRAIN activity, and parental behaviors [19]. The relaxation and safety present in attachment is facilitated by the parasympathetic nervous system [20]. This system works in opposition to the sympathetic nervous system, which is responsible for the stress and excitement associated with attraction. The parasympathetic nervous system is regulated by oxytocin, which reduces stress through the inhibition of our fear response [19]. In other words, attraction can be enhanced by the body’s stress response while attachment inhibits those anxieties.

In addition to its role in the parasympathetic nervous system, oxytocin is associated with processing and retention of social cues [13]. For instance, Rohan’s attachment to Charlotte makes him very perceptive of subtle changes in Charlotte's behavior and mood that may go undetected by others. This attachment between Rohan and Charlotte is similar to attraction due to the increased presence of dopamine in both stages. Specifically, the differences in activation of the brain regions which play distinct roles in the facilitation of attraction and attachment, like the dorsal anterior cingulate cortex (dACC) and posterior cingulate cortex (PCC), are modified over the course of this transition between attraction and attachment. The dACC helps process information and facilitates decision making based on the context of social interactions [20]. The PCC contributes to increased social awareness and trustworthiness in the progression of romantic love [21, 22]. During the attraction phase often present in short relationships (one to seven months), activity in the dACC and PCC is low. As a relationship transitions to the attachment stage (eight to seventeen months), increased activation in the dACC and PCC is associated with the suppression of obsessive thinking [23]. These anxious tendencies disappear around six months after initially falling in love; therefore, alterations in dACC and PCC activation may help explain these changes [13].

LUST, ATTRACTION, AND ATTACHMENT: I WANT TO KNOW WHAT LOVE IS

other hand, motivates infatuation with a person via the sympathetic nervous system and the release of dopamine. These stages precede attachment, which characterizes secure commitment to a significant other due to the parasympathetic nervous system, the release of oxytocin, and activation in the dACC and PCC. Charlotte and Rohan experience lust, attraction, and attachment together; however, these three systems can exist independently from one another as well. For instance, Charlotte finds her local barista handsome, yet has no emotional attachment to him. On the other hand, Charlotte may feel attachment towards her best friend without feeling sexual attraction towards her [24]. If lust, attraction, and attachment can be functionally independent, why do they so often occur simultaneously? Attachments are most likely to form between individuals that have extensive contact with one another over prolonged periods of time [16]. Lust and attraction provide grounds for this extended contact, increasing the likelihood that one becomes emotionally attached to sexual partners [16].

Not to mention, sex can be a means of expressing attachment to one’s partner, as physical intimacy releases oxytocin and can aid the development of emotional connection [8].

More broadly speaking, social beliefs about romantic relationships may help explain why we fall in love with the people we are sexually attracted to. People may believe that lust, attraction, and attachment all exist together under the umbrella concept of ‘love’ [25]. This assumption may be connected to the social importance of finding a lifelong romantic partner and the ostracization of those who decide to stay single or refuse to commit to a single partner [26]. Such interactions between neurological and social mechanisms contribute to the complexity of human relationships and our conception of love as a whole.

References on page 49.

Although they all exist as forms of love, lust, attraction, and attachment each possess their own qualities and serve different functions. For instance, lust is primarily associated with the initiation of sexual activity through hormone production and reduced activity of the prefrontal cortex. Attraction, on the

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THE BRAIN-COMPUTER DEBATE

THE BRAIN-COMPUTER DEBATE: IS THE HUMAN BRAIN LIKE A COMPUTER?

by Daniella Lorman/ art by Ava Sclafani

n the late 1940s, pioneering comIwhat puter scientist Alan Turing asked it would take for a machine,

or a computer, to think for itself.

Turing predicted that, by the year 2000, “one will be able to speak of machines thinking without expecting to be contradicted” [1].

Turing’s comment was admittedly a bit optimistic. Now, over seventy years later, there is debate amongst philosophers, neuroscientists, and computer scientists regarding the similarities between the brain and a digital computer [2, 3]. If machines could theoretically ‘think’ and process information like the human brain, would this mean that human brains process information like machines?

To begin answering this question, let’s delve into the architectural differences between a typical digital computer and the human brain.

TRANSISTORS VS. NEURONS: HOW DO COMPUTERS AND BRAINS COMPARE? Our first instinct may be to think of a computer as a consumer device such as a Mac, a PC, or a smartphone. However, a plethora of different computer types exist, ranging from the most primitive analog computers to massively complex quantum computers. According to some neuroscientists, a computer is generally any system that transmits signals, integrates information, and converts inputs into outputs [3]. While the

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THE BRAIN-COMPUTER DEBATE

brain and the computer both process information, defining a computer as something that receives information, manipulates it, and determines outputs does not account for the embodied nature of a human brain, nor the impacts of external processes and environmental factors on cognition. Modern computers are largely based on the Von Neumann architecture, first developed in 1945 [4]. A Von Neumann based computer uses a single central processor (CPU), which loads and executes instructions, as well as a memory unit that holds instructions and data. There are also peripherals, or output devices that send data to human users or other computers. The CPU, memory unit, and peripherals are all connected via communication systems known as ‘buses.’ A computer constructed around the Von Neumann architecture processes information sequentially, following the specific order of instructions encoded in the memory unit [4].

In contrast to Von Neumann based computers, the human brain engages in parallel processing, or the processing of multiple tasks continuously and allat-once [5]. Most sensory and motor system neural pathways, for example, intercept several brain regions. Even within each brain region, there are multiple neural networks that operate at the same time. In this way, the human brain’s architecture differs from the more rigid Von Neumann model, in which information is processed in discrete, sequential intervals. Notably, however, computer systems that process in parallel do exist, such as those with more than one processing unit.

In fact, modern technologies like the iPhone implement parallel processing.

Before taking a position in the debate, it’s imperative to consider prevailing arguments considering the structure of the human brain relative to a computer.

Some academics have argued that the biological brain functions as a massive parallel computer [6]. For example, computer scientist Marvin Minsky argues that the human brain is formed by several ‘agents’ — akin to the transistors in a computer — each of which is mindless [7, 8]. Together, these ‘agents’ create the mind by processing information simultaneously [7].

Others broadly define a computer, arguing that both the brain and the computer essentially complete the same task: information processing [3]. In addition to the many philosophical arguments conceptualizing the human brain, the inability to isolate what in particular contributes to parallel processing in the human brain poses an obstacle in drawing comparisons.

Several computational models have been employed to study or attempt to simulate the parallel processing characteristic of the human brain, yielding results suggesting that parallel processing of various tasks in the human brain occurs at the level of neural regions rather than individual neurons themselves [5]. However, many questions remain unanswered regarding the precise role of individual neurons, neuronal connections, and structural regions that contribute to parallel processing in the human brain. For example, we have not yet been able to determine just how many processes the human brain is capable of processing at the same time [5]. Until the precise mechanism of parallel processing within the human brain is elucidated, equating the human brain to a computer may be an apples to oranges comparison.

THE IMPACT OF EXTERNAL PROCESSES ON COGNITION A fundamental difference between the human brain and a device — such as a digital computer — is that the brain’s functioning is inherently dependent on its attachment to and integration with the body. This theory, known as embodied cognition, posits that cognition is shaped by the physiology of the entire organism [9]. Considering the brain as a computer may obfuscate the fact that a brain is still a wholly active biological organ, part of a larger body that interacts with the surrounding environment. Consequently, the brain and its cognitive abilities are subject to a plethora of diseases and environmental factors, both of which impact the human body. When considering the structure of the human brain as a computer, philosophers often focus solely on the role of neurons in cognition and

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THE BRAIN-COMPUTER DEBATE information processing, commonly comparing neurons to transistors, or the electronic devices within a computer that regulate electric current [3, 7, 10].

But, the neuroscientific reality is that there is much more to the functioning of a human brain than the contribution of neurons.

Another major cell type in the nervous system occupies over half the volume of the human brain and is far more numerous than neurons: glial cells. Glial cells are non-neuronal cells that, unlike neurons, do not produce electrical impulses. A variety of glial cell subtypes exist — including astrocytes, oligodendrocytes, and microglia — and the functions of each glial cell type are similarly diverse. Astrocytes remove waste material and interact with the brain’s extensive vasculature to provide cells with nutrients. Further, astrocytes maintain brain homeostasis by modulating the chemical environments in the brain that are critical for communication, or signaling, between neurons [11]. For example, astrocytes modulate the recycling of the primary excitatory neurotransmitter in the brain, glutamate. Glutamate is crucial in regulating learning and memory processes, but dysregulation in glutamate processing is widely correlated with the progression of neurodegenerative diseases [12, 13]. In this way, astrocytes are directly involved in the facilitation of learning and memory processes in the brain [12, 13]. Oligodendrocytes are responsible for creating and maintaining the myelin sheath in neurons, a ‘sleeve’ of insulating material surrounding neurons that allows for quicker electrical signaling or communication between neurons. Similar to astrocytes, when oligodendrocytes are compromised and unable to produce myelin sheath, they contribute to the pathology of neurodegenerative disease [14]. Finally, microglia maintain neural networks by responding to injury, inflammation and pathogens.

As such, microglia are commonly referred to as the ‘immune cells’ of the brain.

in the brain. These abnormal tau proteins form tangles by clinging to other proteins in the brain, and may even build up within astrocytes. Another hallmark of Alzheimer’s disease is the accumulation of aggregates or plaques of a protein called beta-amyloid. Together, tau tangles and amyloid plaques disrupt neuron function and contribute to cell damage and death [15, 16, 17]. A common thread across neurodegenerative conditions is that their development has little to do with a single neuron [18]. Rather, while a dysfunctional non-neuronal cell or protein results in damage to the neuron itself, pathways of neuronal connections are required to propagate electrical impulses. As a result, there is limited use in investigating the role of solely one neuron in modulating cognitive processes [18].

At first glance, some may consider glial cells and tau proteins to be internal factors, or components of the human brain’s broader information processing system. After all, these structures exist in the brain and influence neuronal functioning. In the ‘brain as a computer’ metaphor, neurons are often equated with the transistors that make up the computer’s combined information processing components (the central processing unit and memory). However, in the computer, there is no substance or mechanism that is immediately analogous to that of a glial cell, tau tangle, or beta-amyloid plaque. Using this foil, we can see that glial cells and tau proteins can impact cognition by impacting neurons, but they appear to function externally to the brain’s system of information processing.

This marks one of the major differences between a biological brain and a computer; cognition in the human brain is impacted by biological factors outside of the immediate information processing system. In the inorganic computer, these factors are simply not present.

In addition to glial cells, abnormal cell types may arise in the human brain, such as in instances of neurodegenerative disease [15, 16, 17]. For example, individuals with Alzheimer’s disease experience an abnormal buildup of the tau protein, which c o nv e nt i o n a lly helps stabilize the internal skeleton of neurons

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THE BRAIN IS A BIOLOGICAL ORGAN. A COMPUTER IS NOT. Let’s consider a seemingly obvious statement: the brain is a biological organ, while the computer is a digital system. Conceptualizing the human brain in relation to a digital system is difficult [2, 3]. As a biological organ, the brain has a natural evolutionary history that has forged its

THE BRAIN-COMPUTER DEBATE structure and function, in tandem with the body.

Computers, on the other hand, have advanced through developments created by human scientists and software developers; as it stands, computers cannot yet fully program themselves or evolve via a system comparable to Darwinian evolution [19]. For instance, Microsoft Windows cannot identify, troubleshoot, or repair errors or shortcomings in its own code, nor can it organically ‘evolve’ into the next, more ‘fit’ version of Windows.

Diseases and disorders occurring outside of the brain can impact its functioning and cognition [20]. Syphilis, a disease stemming from a bacterial infection, commonly begins with a small lesion. If left untreated, syphilis can transform into a systemic, long-term disease with devastating physiological consequences. In some instances, neurosyphilis, or the spread of the disease to the central nervous system, may develop. Patients with neurosyphilis commonly experience dementia, cognitive impairment, mania, and psychosis as the disease ravages their central nervous system [20].

Syphilis is a disease with biological origins outside of the brain that causes the degeneration of neurons. Importantly, syphilis is not caused by the brain; rather, the brain becomes involved as a consequence of its embodied nature.

Computers, like a human being, can also contract viruses. A computer virus works by replicating itself to modify and damage the functioning of computer programs. Oftentimes, viruses cause critical damage to the functioning of the computer’s operating system or cause specific programs to cease working. Computer viruses are vastly different from the pathogens that infect living beings. For instance, neurosyphilis impairs cognition by physically damaging the structure of the brain and the CNS [20].

Computer viruses rarely impact the physical architecture of the computer itself, and instead only infect programs such as the operating system. In some rare instances, computer viruses may physically damage the computer by infecting its firmware, causing internal cooling systems to fail. However, the large majority of computer viruses do not affect the architecture of the transistors, CPU, or memory.

When a pathogen impacts the human brain, its analogous information processing systems are physically damaged.

Beyond pathogens, organ dysfunction and conditions including improper blood sugar levels or hor-

monal imbalances can impact cognition [21, 22, 23].

Chronic kidney disease, which results in the kidneys being unable to properly process and filter toxins from the blood, contributes to cognitive decline by damaging cerebral vasculature [21]. Transplanting one’s failing kidneys improves performance in verbal and visual memory, spatial reasoning, processing speed, and general cognitive status [22]. The effects of kidney dysfunction on cognition represent yet another external, non-neuronal factor that impacts cognitive processing. In a computer, there is no function immediately analogous to the intertwined nature of the body and cognition. Installing additional computer memory and upgrading a hard drive are all ways in which we can improve a computer’s performance, but can we equate this to that of replacing a failing organ in the human body? Or treating a disease that impacts cognition? Components such as the memory unit, central processing unit, and hard drive are — according to Von Neumann architecture — essential to the computer’s ability to process information. These are not external structures, like the kidneys or liver; rather, they are internal components of the computer’s ‘brain.’ Would it, therefore, be possible for a human brain to process information if separated from the body?

THE BRAIN IN A VAT PROBLEM Envision a hypothetical — and highly unethical — experiment in which a scientist removes a human brain from its body and suspends it in a vat of self-sustaining fluid. The brain’s neurons are then individually wired to a supercomputer that produces electrical impulses identical to what the embodied brain would

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THE BRAIN-COMPUTER DEBATE receive. This hypothetical experiment, known as the ‘brain in a vat’ (BIV) scenario, was conceptualized by philosopher Gilbert Harman to question our conceptions of knowledge, mind, and consciousness [24, 25].

In the BIV scenario, the disembodied brain would continue to have experiences analogous to those of an embodied brain, despite its detachment from the human body [24, 25]. However, if the brain is separated from the body, it cannot process stimuli that it would receive from the body. This idea that cognition arises from dynamic interactions between an organism and its environment is known as enactivism [26]. Enactivist theory posits that organisms do not passively receive information from their environments, such as the brain in the vat would; rather, that natural cognitive systems enact a world by participating directly in the generation of ‘meaning’ [26]. Therefore, in line with enactivist theory, the body is an essential component of cognition, since it is the agent that interacts with the environment.

Computers, on the other hand, are tasked with information processing. When a computer parses through a function, it does not assign meaning to that function. When our brains are tasked with processing seemingly arbitrary stimuli — such as interpreting fluctuating sound frequencies as spoken language, or the intangible social meanings we derive from interpersonal interactions — these interactions seem to translate into ‘meaning.’ Of course, there are non-biological devices, like a thermostat, that seemingly react to external stimuli. But, the action of a thermostat adjusting its temperature when it detects that a room is too hot, lacks intent. The thermostat, unlike a brain, does not care about its

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own survival, nor does it ascribe meaning to the factors in its environment. However, the human brain, as a component of a larger body, does not process information passively like that of a computer’s central processing unit.

The human brain is also not a device, like a thermostat, that responds to environmental stimuli without intent or ascribing meaning. Rather, the brain is one component of a dynamic biological system: the human body.

“MEAT” VS. SILICON Even a parallel computer — which seemingly processes information in a manner which resembles that of a biological brain — is not embodied. One fundamental difference between the human brain and a computer lies in the brain’s function as just one component of a larger biological system; it is influenced by and dependent on stimuli that the body encounters. A computer, on the other hand, is a standalone information processing system. Unlike a brain, it is not enactive.

A computer may not interact with its environment in the same way that the human brain can, nor may it be able to derive meaning from its environment. In the decades since John von Neumann first developed the fundamental architecture of the modern computer, computers have transformed from room-size IBM mainframes to highly advanced and ubiquitous elements of our day-to-day lives. So, is the human brain like a computer? There’s much to consider and several questions to ask before we may resolve the controversy.

References on page 50.

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GRIEVING A CHANGING ENVIRONMENT

GRIEVING A CHANGING ENVIRONMENT: EXPLORING THE EFFECTS OF CLIMATE CHANGE ON THE PSYCHE

by Jaclyn Narleski/ art by Arden Spehar Oh, but you know, climate change doesn’t ex‘everything ist.’ This all-too-familiar phrase is prevalent in from casual conversation to national media, despite increasing evidence demonstrating its fallacy. Climate denialists claim it’s a ‘liberal fabrication’ and ‘the climate is supposed to change anyway,’ leaving aside the clear evidence of its increasing effects. It’s a narrative that’s pervasive and often politically charged in the greater conversation surrounding climate change. However, there is another perspective and experience that is just as real. Those who believe in climate change, and/or experience it themselves, can suffer negative mental health effects. Neurophysiological deficits and disorders can also arise from the stress of climate change –– a type of stress becoming known in some circles as ‘solastalgia’ or climate grief. Despite the impacts of climate change becoming more and more visible, a gap in understanding still persists between climate effects and mental health.

THE ORIGINS OF SOLACIUM ALGOS Solastalgia is defined as the feeling of distress that arises from environmental changes or prolonged anticipation of environmental changes.

The term is derived from the Latin root words solacium, meaning solace or comfort, and algos, meaning desolation or pain [1]. While solastalgia may sound similar to nostalgia, it was not coined just to describe the feelings of longing or melancholy experienced when losing something one loves. In reality, it also describes the feelings of distress in response to changes in a particular environment — especially for people who have a direct connection to that environment [2]. Populations that are directly connected to their environment are typically those whose lifestyle, culture, personal iden-

tity, or community relies directly on the geographical, vegetative, and climatic features of their home [3]. For example, the Afar and Borana Indigenous communities of Ethiopia rely directly on the land for raising livestock, farming crops, and other resources. The worsening effects of climate change have caused a grazing land shortage, recurring droughts, increased

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GRIEVING A CHANGING ENVIRONMENT flooding, and more resource-based conflicts [4].

When populations like the Afar and Borana people experience firsthand changes to their environment, they may experience solastalgia. Such changes can also include natural disasters like volcanic eruptions, hurricanes, or snowstorms, as well as anthropogenic — or man-made — changes, like deforestation, oil spills, or mountain blasting. Additionally, anthropogenic climate change can, in turn, cause environmental changes such as increases in hurricanes, snowstorms, and drought, as well as shifts in temperature [2]. The consequences of these natural or man-made environmental changes can also affect mental health [5].

The term ‘solastalgia’ was first coined by philosopher Dr. Glen Albrecht in 2003, and has since been widely used in academia as interest rises in the mental and emotional impacts of environmental change [6]. In the past five years, the effects of climate change have grown exponentially, leading to an increase in media coverage documenting both individual and shared experiences of these environmental changes. As mental health challenges caused by climate change have become more commonplace, there has been a surge in research illuminating the struggles that individuals experiencing solastalgia navigate [6]. As such, the term ‘climate grief’ was dubbed to describe the feelings of distress that frequently accompany the anticipated loss of ecosystems, land, species, or ways of life [3]. While some populations may experience solastalgia because of their direct connection to their environment, others may experience distress over the mere anticipation of the vast

effects of climate change, man-made destruction, or natural disasters.

TO FIGHT OR TO FLY: STRESSING ON SOLASTALGIA Grief is a universal response to a loss or separation from someone or something we love [3, 7, 8]. Solastalgia and climate grief both describe emotional responses to losing, or anticipating the loss of one’s home or way of life due to severe environmental damage [2].

While solastalgia and climate grief are the overarching concepts that encompass emotional responses to environmental loss, more specific subtypes of these responses have been named to further describe specific situations and feelings that accompany climate change [9]. These subtypes are known as eco-grief, eco-anxiety, and eco-guilt [9].

Eco-grief, which is similar to climate grief, characterizes the feelings of anger or sadness that arise from the loss or anticipated loss of one’s physical environment [9]. For example, someone might feel angry and frustrated when experiencing an abnormally consistent drought that limits their water supply. Eco-anxiety encompasses the feelings of worry that arise from considering either the future of climate change or how future generations will experience its damage, as well as the distress of knowing others may suffer from environmental harm [9]. This subtype describes the symptoms commonly associated with anxiety and depressive disorders, such as an inability to sleep, socialize, or work, that arise as a result of changes in one’s surroundings [10]. For instance, a mother might have difficulty sleeping because she is extremely anxious about how climate change will impact her children’s lives. Eco-guilt describes the feelings of individual responsibility, self-blame, or dissatisfaction with oneself or one’s generation as related to climate change [11]. For example, a commuter might feel guilty for driving to work every day, feeling personally responsible for the carbon emissions put into the atmosphere from their car. Each subtype defines various feelings of distress that come from lived experiences of environmental degradation, and each can develop into distinct psychological issues.

Solastalgia can occur simultaneously with, or result in, other psychological disorders such as post-traumatic stress disorder (PTSD) or mood disorders like depression [11]. PTSD can manifest from experiencing a life-threatening event, like a natural disaster, that causes death, major injuries, loss of resources, or relocation from home, while anxiety disorders or depression can occur as a result of other types of change as

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GRIEVING A CHANGING ENVIRONMENT well. Prolonged environmental changes, or even the anticipation of environmental changes, can result in mood disorders. Some examples of transformation include extreme heat waves, glacial spells, droughts, floods, or the extinction of species. Aggressive behavior, substance abuse, and suicide rates have also been shown to increase with environmental disruption [11, 12].

Prolonged depressive responses like grief, stress, and anxiety can cause neurophysiological changes.

Solastalgia and climate grief are commonly recognized as depressive responses, and individuals experience similarly high levels of stress when experiencing solastalgia as they might when experiencing depressive responses [11, 13]. Those who experience solastalgia or climate grief may experience an inability to regulate their levels of a stress hormone called cortisol [14]. Cortisol activates the body’s fight-or-flight stress response by releasing sugars into the bloodstream and increasing heart rate and blood pressure [15]. Continuous activation of the fight-or-flight stress response from the uncertainty and threats that environmental changes pose can cause sleep disturbances and negatively impact the immune system’s ability to function [14]. Negative impacts on the immune system’s functionality can make one more susceptible to infectious disease [16]. Experiencing chronic stress can also have negative effects on cognitive performance because it can cause the brain to atrophy [17, 18]. A few examples of negative effects on cognitive performance include a decrease in attention span, difficulty retaining memory, or struggling to problem-solve [18].

Additionally, feelings of helplessness and lack of control that commonly arise from solastalgia or climate grief can inhibit one’s motivation or ability to interact with others and perform daily tasks [14]. In turn, these neurophysiological effects of solastalgia and climate grief can influence our behavioral responses toward climate change and its effects.

DESPAIR, DEFER, DENY: CLIMATE ACTION AND SOLASTALGIA Solastalgia can cause several emotions — fear, anxiety, stress, insecurity, powerlessness, etc. — that affect a person’s relationship not only with their unstable environment but also with themselves and others [19]. Solastalgia often brings about guilt and a sense of personal responsibility for the causes and effects of climate change, leading to behavioral responses to relieve those feelings. In other words, one may feel as if they are responsible for their changing environment [9, 19]. This combination of guilt and personal responsibility can impact behavior in two different ways. It’s important to note that regardless of where responsibility lies on the societal level, on the individual psychological level, these are the responses that someone affected by solastalgia or climate grief may exhibit. In the attempt to eliminate their individual impact, one might make drastic lifestyle changes like converting to veganism, saving extensively-used products, or using candlelight to save on electricity.

Alternatively, someone might defer the responsibility of climate change as a defense mechanism, allowing them to relieve whatever intense stress, conflict, or anxiety they are experiencing [9, 20]. They might place blame on older generations, larger corporations, or governmental actions, rather than taking responsibility themselves. These defense mechanisms can evolve into full-blown climate change denialism in order to decrease experienced guilt or stress [20]. People may also choose to isolate themselves from social activities, which may result in diminished social support from a community [3]. Just as individuals are impacted by solastalgia and climate grief in these ways, entire communities can collectively experience negative effects.

READING THE LANDSCAPE: EFFECTS OF SOLASTALGIA ACROSS COMMUNITIES AND CULTURES

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GRIEVING A CHANGING ENVIRONMENT Solastalgia can be triggered by varying pressures of environmental change and the dread that arises from anticipating worsening conditions [3]. There are three main categories of loss that can evoke solastalgia or climate grief: acute physical ecological loss, disruption of sense of place, and anticipated future loss. Natural disasters or extreme weather events are considered acute physical ecological loss [3]. ‘Sense of place’ refers to the distinct characteristics and emotional attachments people experience in terms of place [21]. The disruption of one’s ‘sense of place’ and personal identity with respect to their environment is considered a loss of environmental knowledge. Finally, there’s the anticipated future loss due to environmental changes [3].

Let’s consider a real-world example that explores these three types of loss. Mount Merapi is an active volcano located in central Indonesia. In the last 3 decades, the volcano has erupted multiple times, most notably in 1997, 2006, and 2010 [22]. Due to these frequent eruptions, nearby communities like the Cangkringan village experience solastalgia from the anticipation of losing their environment in the near future [23]. Those who had already witnessed an eruption during their lifetime may be especially distressed because they already had to adjust their lifestyle, cultural practices, or simply no longer felt comfortable in their altered environment [23]. The 2010 volcano eruption of Mount Merapi, in particular, severely affected the Cangkringan village and other surrounding villages in the volcano’s reach [25]. Approximately 2,200 families were displaced from the damage to their homes and 400,000 total people were internally displaced because of the dangerous lava flows that resulted from the eruption; this is an example of acute physical ecological loss [24]. Due to the destruction and displacement caused by the volcanic eruption, residents showed pronounced solastalgia because they no longer felt safe and comforted by their home environment and were physically removed from their homes [25]. Ad-

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ditionally, Indonesian residentcontinued to experience distress even two years later, as farms, roads, housing, and rice fields still remained extensively damaged. After experiencing acute physical ecological loss, the Cangkringan village people felt a disruption to their ‘sense of place.’ Volcanic dust coating the roads served as a constant reminder of the damage that had ensued, and made the surrounding environment seem foreign. Construction activity and modifications to farming practices also contributed to the disruption of sense of place, because it required potentially major lifestyle changes [25]. Even a slow disruption to sense of place can cause stress just as great as one as sudden as a volcanic eruption.

‘We used to read the landscape. But now it changes, you have to guess now. Everything changes, [making] it so hard… You never know, it just change[s] like that, even the tide… Like before, you know what [was] gonna happen. So hard now, guessing all the time, through [the years] from 2000 [it] is sort of getting worse. I think it start[ed] changing in the 1980s, the changes start[ed]… [I] am sad at home, think[ing] about the good old days, we always talk about the good old days. Now everything is changing, even the trees, you can see changes in them, even the fruits, like before, we haven’t had mango season’ [26].

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GRIEVING A CHANGING ENVIRONMENT Expressing their own solastalgia, residents from Erub Island, Australia, a region devastated by rising sea levels, recounted their experience with anguish.

Just from minute changes to their surrounding environment, residents of Erub Island felt sadness and fear in the face of such change as it threatened their sense of place [26]. They may also experience eco-anxiety in anticipating the future loss of their sense of place as these changes continue to occur.

Climate change affects us all. However, the threat to our ‘sense of place’ and development of solastalgia or climate grief can vary between ecosystems and communities. Certain groups are potentially more vulnerable to solastalgia — like Indigenous peoples, farmers, mountaineers, people with disabilities, people of color, older people, women, and children [3, 5]. For example, the Fulani people of Nigeria, Africa experience greater solastalgia from changes to their environment due to their dependency on the land that facilitates their way of life [4]. Younger adults have also shown to be more susceptible to climate grief because of the generational pressures that have been placed upon them [10]. Generational pressure comes from older communities off-loading the responsibility of resolving the issue of climate change onto younger communities [10]. In addition to this pressure, these younger communities concurrently grapple with climate grief, which exacerbates the stress from pre-existing issues like food insecurity, overcrowding, and poverty [3]. Disruption of ‘sense of place’ can present differently in wide-ranging communities and groups of people, but as the effects of climate change increase in severity, it will become a familiar feeling to us all.

LOOKING BACK AND MOVING FORWARD The mental health effects of environmental change are real and pressing to society as the threat of climate change continues to grow. These effects manifest in numerous psychological issues, including depression, anxiety, and chronic stress, that can influence our behavior towards environmental change. Individuals can develop behaviors and attitudes towards climate change that reflect their need to relieve themselves of said stress or other negative feelings. It’s important to acknowledge, however, that everyone experiences different forms of loss and environmental change, and may maintain unique relationships with their environment. The effects of solastalgia will impact certain groups disproportionately, especially those who have a direct connection with their natural environment and value sharing their space with it.

Climate change is an ongoing issue that will continue to grow in severity if humanity refuses to take meaningful steps to fight it. Those not directly affected by the current consequences of climate change are often reluctant to push for change, reflecting a human-centric perspective versus the environmental perspective we need. Nevertheless, as the effects become too large and frequent to ignore, the distress of experiencing and anticipating it all could motivate a greater effort to fight climate change. Perhaps then, we might make some headway in the right direction.

References on page 51.

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HYPOXIC CONDITIONING

HYPOXIC CONDITIONING: WHEN LESS (OXYGEN) IS MORE

by Alex Roth/ art by Anna Bishop 24

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HYPOXIC CONDITIONING hat comes to mind when you think of the mounW tains? Is it hiking? Snow? Bighorn sheep? Alzheimer’s Disease…? Alzheimer’s Disease (AD) might

not be the first thing that comes to mind when you think of the mountains. However, AD-related deaths have been shown to decrease as altitude increases and, correspondingly, air pressure and oxygen levels decrease [1]. At first glance, there is no obvious link between altitude and AD mortality, but what if the connection between lowered air pressure and AD could be revolutionary in the management of this disease that affects 30 million people worldwide [2]? Enter hypoxic conditioning: an emerging preventative treatment for a number of conditions including neurodegenerative disease, stroke, and heart attack [3, 4, 5]. Hypoxic conditioning (HC) is a treatment that trains you to resist lowered oxygen levels in your body, a state called hypoxia. Experiencing hypoxia causes the body to react by trying to obtain more oxygen and defaulting to other ways to make energy, which may make one feel lightheaded or groggy. Like a vaccine that introduces small amounts of a disease to train your immune system’s resistance, HC deprives you of oxygen for short periods of time to train your body to withstand hypoxia. Over time, this reaction results in a vaccine-like resistance to the sustained hypoxia seen in many diseases related to aging.

AD is part of a group of neurological illnesses known as neurodegenerative diseases, which cause deterioration and death in the cells of the brain and spinal cord. This degeneration causes dementia, which is classified as the loss of multiple mental functions including memory, reasoning, normal personality, and language [6]. AD is the most common cause of dementia, which can appear subtly over many years and be extremely debilitating [2]. AD is the sixth leading cause of death worldwide, largely due to ineffective treatment options that fail to address the full scope of the disease [2, 7].

YOUR BRAIN ON HYPOXIA To understand how diseases like AD affect us, we must first understand how our brain’s metabolism works. The keystone of our body’s energy production is the mitochondrion, often known as the ‘powerhouse of the cell.’ The mitochondrion converts the body’s fuel — glucose — to energy, and stores it as adenosine triphosphate (ATP), the universal energy currency for biological systems. The mitochondria can be thought of as cellular engines, since they use a constant flow of fuel and oxygen to maintain ATP

production rates. Your body usually generates energy using oxygen through a pathway called aerobic respiration [8]. However, even if you are breathing enough oxygen from the air around you, it may not be properly distributed to different areas of your body, causing hypoxia in these areas. Hypoxia forces the body into a different type of respiration: anaerobic respiration. Though it uses no oxygen, this method of energy production generates substantially fewer ATP per glucose molecule [5]. Furthermore, anaerobic respiration results in the overproduction of mitochondrial byproducts called reactive oxygen species (ROS), which damage cell structures and processes. ROS molecules can cause neuroinflammation, the brain’s ‘scorched earth’ immune response against the damaged cellular architecture that results in widespread damage to the brain. If your brain is forced into anaerobic metabolism for too long, neurodegeneration and cell death begin to occur [5].

The brain requires large amounts of energy to function effectively: it uses one fifth of all the oxygen in your body and one fourth of the glucose. When there is plenty of oxygen present, it prefers the greater efficiency of aerobic metabolism [8, 9]. In some instances, however, our bodies lack the oxygen required to undergo aerobic metabolism. Following a period of intense exercise, your brain enters a state of hypoxia. As

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HYPOXIC CONDITIONING a result, you may feel lightheaded, confused, tired, anxious, uncoordinated, and clumsy [10, 11]. These sudden changes are a result of your brain failing to keep up with its energy production needs, causing cognitive function to temporarily deteriorate. Hypoxia is particularly dangerous for the cells of the brain, or neurons, because they have higher energy requirements than other cells [5]. Fundamentally, the body needs two main ingredients for sustained energy production: glucose and oxygen. However, during hypoxia, there is not enough oxygen for sustained aerobic metabolism, so the body switches to anaerobic metabolism.

A WORKOUT FOR YOUR BRAIN: THE PRINCIPLES OF HYPOXIC CONDITIONING Since the body prefers anaerobic metabolism in hypoxic conditions, the idea of HC might seem perplexing [8]. How could repeated exposure to a dangerous state be safe, let alone helpful? Let’s take a look. Like athletic conditioning, HC uses short ‘workouts’ for your metabolism, which activate hypoxic defenses against diseases like AD. Over time, these ‘workouts’ help the body endure low oxygen levels. Just as a runner jogs every day to prepare for a marathon, HC would expose people to controlled periods of hypoxia, conditioning them against metabolic disease [12].

A marathon runner on their morning jog needs more blood pumping to their leg muscles than if they were resting, so their heart rate may increase for the duration of their run. Similarly, our brains have evolved a number of short-term defenses against oxygen deprivation, which have the potential to be advantageous when implementing HC [13]. Without these defenses, brain cells would quickly lose function and eventually die. One such defense is an initial upregulation of aerobic metabolism, which sustains the brain by generating as much ATP as possible while some oxygen still remains [14, 15, 16]. The brain also increases anaerobic metabolism as a backup strategy to continue producing a small amount of energy [15]. A number of proteins that modulate our body’s responses to hypoxia, termed hypoxia inducible factors (HIFs), are activated as well [5]. Activation of HIFs ‘turns on’ antioxidant molecules that help neutralize ROS byproducts by dampening their ability to damage and inflame the brain. Finally, the brain increases its glucose intake to refuel its cells [17]. The promise of HC lies in how it leverages these defenses. Instead of simply activating these mechanisms for short-term protection, HC promotes the

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development of a long-term protective state that is resistant to hypoxic damages [13].

Once again, imagine our marathon runner: they may not see immediate improvements in their running, but over time their leg muscles, heart, and lungs will strengthen and grow to support their body as they run. Similarly, repeated bouts of HC help the brain become more resilient in the face of long-term oxygen deprivation, decreasing potential damage to brain cells. HC stimulates new growth of blood vessels, enabling future increases in blood flow and thereby supporting glucose and oxygen delivery to the brain [17].

The brief disturbances HC causes in the brain’s oxygen levels also train the brain to better resist disruption of ATP generation [18, 19]. Finally, HC activates protective antioxidant mechanisms — including HIFs — against long-term ROS production [20]. Activating these defenses helps prevent the damages that hypoxia and subsequent decreased metabolism can cause [21, 22, 23]. Now, under the duress of hypoxia, the brain can rely on not only its standard defenses, but also its newfound resilience resulting from HC. However, HC does have the potential to damage the brain [24].

Just as runners must be careful to avoid injuries from overtraining, the duration of hypoxia needs to be carefully controlled during HC to keep the brain safe from injury [22, 25]. Fortunately, oxygen can be delivered at intervals that both induce the benefits of HC and keep the patient safe [22, 25]. In doing so, healthcare

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HYPOXIC CONDITIONING providers can take advantage of HC to help the rapidly growing population at risk of AD [26].

INTO THIN AIR: TREATING ALZHEIMER’S DISEASE WITH HYPOXIC CONDITIONING Much like our bodies, our brains also slow and decay with age. In the process, metabolism typically becomes less efficient, which — along with other processes — results in neurodegeneration [27]. The same metabolic alterations responsible for the aging of the brain are also seen in a more advanced form of AD [28, 29]. Decreased blood flow to the brain is thought to be the earliest manifestation of AD [30].

Soon after, mitochondrial and metabolic processes begin to malfunction, hindering the brain’s ability to produce energy [31, 32]. In turn, these malfunctions lead to chronic hypoxia and lowered brain metabolism, both of which are major contributors to the symptoms of AD [33, 34, 35]. Fortunately, the possibility of utilizing HC to decrease the metabolic dysfunction of AD is currently being explored [21, 36].

Though AD has significant non-metabolic components, HC mainly shows promise in its ability to mitigate metabolic deficits [12]. Reduced blood flow to the brain can be used to predict behavioral symptoms like memory difficulties before they emerge [9, 37]. Brain cells in people with AD typically have lower metabolic rates than healthy brain cells, poten-

tially because less oxygen and glucose are being delivered to them through the blood [9, 38]. As a result, brains are forced to rely more heavily on anaerobic metabolism, resulting in damage to brain cells from excessive ROS generation [22, 38]. Remember HIFs — the proteins HC activates? HC can keep HIFs activated for a long time and provide a safe way to activate them before they are needed [5, 39]. When activated by HC, HIFs express red blood cell and blood vessel production genes, thereby increasing oxygen-rich blood delivery to the brain [17, 35]. The addition of new blood cells and vessels is akin to adding more delivery trucks to a mail route; now more oxygen-rich blood can be delivered to brain cells for aerobic metabolism.

Like running a dryer filled with lint, mitochondria start to wear under the neuroinflammatory stress of AD [36]. Malfunctioning mitochondria are a significant metabolic aspect of AD [31, 40, 41]. Mitochondria are essential in generating the ATP needed for brain survival and function. Therefore, processes such as speech, memorization, and planning are all impaired by lowered mitochondrial function, because fewer ATP molecules are available to power the communication between neurons [42, 43]. HC fortunately shows promise in alleviating mitochondrial dysfunction, as it can stabilize malfunctioning mitochondria and increase growth in lab-grown cells [18, 35]. Furthermore, mitochondria in hypoxically conditioned rats exhibit elevated antioxidant activity and resistance to hypoxia [35]. Perhaps most surprisingly, HC was able to drastically improve survival of mice with experimentally induced mitochondrial disease [18]. Though all untreated mice died by the second month, mice treated with HC only showed mild symptoms by their fourth month [18]! Even though animal results cannot be directly translated to humans, HC appears to limit the effects of mitochondrial disease and dysfunction in model organisms, suggesting a promising future for use in human treatment.

Overproduction of ROS is another major stressor implicated in AD [44]. In a rodent model of AD, ROS were shown to play a role in neuroinflammation and cell death [22]. As a result, neurons exposed to ROS were damaged by the brain’s immune system, leading to cognitive deficits such as impaired memory [22]. Just as a vaccine introduces a weakened version of a virus, the brief hypoxic episodes utilized in HC caused low-level generation of ROS [21]. ROS induce a response that, with reinforcement from multiple phases of conditioning, introduces long-term resistance to ROS damage [21]. The hypoxic ‘vaccine’ effect likely

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HYPOXIC CONDITIONING helps to reduce neuroinflammation by releasing antioxidant molecules and activating other neuroprotective systems [20, 23]. Essentially, HC trains the brain to more efficiently neutralize ROS produced by AD before they can cause neurodegeneration. However, AD is a remarkably complex disease with metabolic and non-metabolic components. Thus, the extent to which HC can act as an effective therapeutic at all stages of AD will remain unknown until human trials occur.

One way AD damage can manifest is in the loss of connections between neurons, which prevents signals from traveling through the brain [32]. Brain cells become vulnerable to damage and death when starved of ATP because they cannot keep up with energetic demands for maintenance and function [27]. In fact, metabolic dysfunction is widely considered to be one of the key factors involved in AD neurodegeneration, as neurons in areas of the brain associated with memory waste away [9, 45, 46]. The goal of HC is to provide a cheap and effective way to restore metabolic and cognitive function, and apply rodent models to human trials to explore its potential as a treatment for sick people in the future.

However, questions remain to be addressed before HC becomes a reality.

[12, 47]. While experiments with animals suggest that there are safe levels of hypoxia to use in conditioning, human trials are still needed to assess HC’s safety and efficacy [22, 25]. Continued research may enable the testing and assessment of both preventative and therapeutic HC treatment in humans for a wide variety of diseases, not just AD [12]. Luckily, HC shows great potential for future advances since it is a novel therapy for neurodegeneration that does not involve expensive, inaccessible medications [48]. As a technique, rather than a physical product, HC could be practiced globally without the need for continuous production and shipping of expirable medication. All these factors may help soften the blow Alzheimer’s disease inflicts on a growing proportion of the elderly population [2].

References on page 52.

One of the most prominent questions which must be confronted before HC can be implemented is what exactly constitutes a safe level of treatment

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DEJA VU

A Glitch in the Mental Matrix: Exploring the Illusion of Déjà Vu

by Dominic Matos and Tamar Paserman/ art by Ming Na Thursday night. You and your boyfriend are celIcalt’sebrating your one-year anniversary at a classy loItalian restaurant. “That’s Amore” by Dean Mar-

tin plays in the background, and a dim, amber light sets the tone. You both browse the wine selection, and end up settling on the rosé. At the same moment, a group of waiters erupt into “Happy Birthday” at a nearby table. Suddenly, a strange sensation comes over you. This night doesn’t seem new anymore. Startled by the tune of “Happy Birthday,” you’re strangely filled with an eerie sense of déjà vu. The lights, the music, the smells… everything feels familiar. “Have we been to this restaurant before?” you ask your boyfriend. “No, it just opened,” he replies. But you swear you’ve seen this before!

A moment later, the feeling disappears, just as abruptly as it came. What is going on?

Déjà vu — or ‘already seen’ in French — refers to the feeling that the current moment has already happened before. It is a strange, nearly universal occurrence, and while centuries of study have yet to fully clarify the neurological underpinnings of déjà vu, it is known that déjà vu-like symptoms can occur in certain forms of epilepsy [1, 2]. This finding, which connects a known biological condition to the ambiguous déjà vu, can provide a glimpse into how the illusion really works. In evaluating déjà vu through the lenses of memory, cognition, and neuroanatomy, we can arrive at a better understanding of its complex nature.

A WALK DOWN MEMORY LANE To understand déjà vu, we must first understand how our memories are processed and retrieved.

Our long-term memory is divided into implicit and explicit memory. Implicit memory is information that does not require active recollection — it is information you just know, like riding a bike or how to navigate through your home. These kinds of

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DEJA VU memories are typically learned through repetition and are effortlessly recalled by your unconscious mind [3]. Explicit memory, on the other hand, refers to the conscious recollection of facts or events.

A category of explicit memory is episodic memory, which consists of specific lived experiences, such as your tenth birthday party or where you left your keys. Though there are different categories of memory, all memory processing and recollection involves the encoding, storage, and retrieval of memories [4]. Encoding is the process of acquiring information and incorporating it into memory, storage is the retention of memories, and retrieval is the bringingto-mind of a previously stored memory [4].

Actively retrieving previously encoded information from your memory storage and reliving the event in your head is known as recollection, and can be thought of as mental time travel. Recalled information includes details and fragments from events, like the color of your childhood bedroom [5]. Familiarity is the related, but distinct, process of recognizing certain stimuli through learned association, such as when you see someone you know and automatically smile. Familiarity is subconscious, felt on a spectrum, and is experienced more quickly than recollection, which is an all-or-nothing phenomenon [5].

Recollection and familiarity are crucial components of explicit memory, since déjà vu occurs when the brain confuses familiarity for recollection [5, 6, 7].

It is also possible for feelings of familiarity to occur without an identifiable source, both in real memories and in déjà vu. For example, when you see a person you know but cannot recall why or how you met them, this could just be ‘poor’ memory, or a case of déjà vu [5]. However, feelings of familiarity can be so strong that a person can believe they are recollecting memories of something they never experienced; this is the eerie feeling you get when déjà vu hits.

in reality, you’ve only experienced the painting. A critical part of a déjà vu experience is knowing that this feeling of familiarity is wrong; you have not experienced the event before, despite the sense of familiarity [9]. Another possible trigger of déjà vu is the configuration of a setting. For example, if your cousin’s living room is arranged very similarly to yours, it could more easily trigger déjà vu than other places. [6]. The more scenes one witnesses — via traveling, dreaming, and watching movies — the greater the likelihood of experiencing déjà vu [6].

NIGHTMARES COME TO LIFE Déjà vu is a complicated phenomenon to study, and while it is hard to pinpoint which parts of the brain are involved, the temporal lobe seems to be the best place to start. The temporal lobe, located in the brain behind our ears, is central to many cognitive functions and, most pertinently, regulates and controls memory storage [10]. Examining individuals with typical versus atypical temporal lobes may elucidate what happens in the brain when we experience déjà vu. For most people —and as in the Van Gogh example —

Déjà vu may be triggered when an appropriate sense of familiarity about one specific element of a situation is misattributed and extended to the entire scene [8]. Say you’ve spent the weekend researching Van Gogh paintings. The next week you walk into a museum and one of his paintings that you saw online is hanging on the wall. You don’t even notice the painting consciously, but your subconscious is familiar with it. Your brain mistakes the familiarity you feel for the recollection of an actual memory, and causes a sudden sense of déjà vu. With sirens of familiarity going off in your brain, you now feel as though you’ve experienced this place before, when

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DEJA VU déjà vu simply refers to an unexplained feeling of ‘I have already seen this before,’ which is known as non-pathological déjà vu. For others, however, déjà vu can occur as a symptom of an underlying disease or neurological abnormality [8]. This kind of déjà vu is defined as pathological [8].

The most common type of pathological déjà vu occurs in those with temporal lobe epilepsy (TLE), which is usually caused by damage to the temporal lobe [1]. TLE is the most common form of epilepsy, a neurological condition characterized by recurring, unprovoked episodes called seizures — sudden, uncontrollable surges of excessive electrical activity in the brain [2]. TLE is typically characterized by impaired long- and short-term memory as well as compromised executive function [2]. When you think of a seizure, you might picture a person experiencing sudden bursts of movement. In reality, this type of seizure is much less common than a typical seizure, which can look more like a person zoning out for a moment [11].

Since individuals with TLE can experience both pathological and nonpathological déjà vu, the neurological bases of déjà vu are commonly investigated through these populations [8]. TLE symptoms manifest in a variety of forms, but the more experiential or hallucinatory symptoms — such as sudden disorientation or intense, spontaneous disconnects from reality — can be referred to as the ‘dreamy state.’ [12, 13] The ‘dreamy state’ is usually accompanied by feelings of déjà vu and strong negative emotions such as anxiety, fear, or general strangeness; one report from a person with TLE describes a vision of a “bald man dressed in black, coming towards her from behind, associated with a feeling of imminent death.” This hallucinatory state encompasses a clustering of various symptoms that may distort one’s consciousness [9]. The experience is associated with temporal lobe seizures and can be elicited by electrical stimulation of sections of the temporal lobe, like the amygdala and hippocampus — brain regions involved in memory processing [14].

People with TLE are more likely to report their déjà vu experiences, which can be intense, visceral, and out of the ordinary, with a wide range of possible presentations spanning from a simple sense of familiarity to an immersive state full of overwhelming emotions [15, 16]. During ‘dreamy states’ simulated via electrical stimulation, people with TLE have recounted experiences like reliving the past while still

being conscious and able to “see [the present] clearly … as if what is happening now has already happened … like an old memory that I am in the middle of living out” [17]. Reliving a memory while also being conscious of the present is a central and curious aspect of the dreamy state [15]. People also often describe the dreamy state as being similar to dreaming even though they are awake and alert. Some memories experienced during the dreamy state are perceived in the third person as a spectator: one patient describes seeing themself “playing the drums, with people from [their] family listening” [15] when in this state. Individuals also often report experiencing déjà vécu in the dreamy state, an experience similar to déjà vu but can last much longer [17]. Déjà vécu can be described as a feeling that one has already lived through entire sequences of events, though these sequences do not start and stop as abruptly as déjà vu. When we experience déjà vu, typically our brain quickly dismisses the feeling as an error, but in cases of déjà vécu, the feeling persists, and the line between illusion and reality starts to blur [17]. For example, an individual with déjà vécu and seizures in the temporal lobe was convinced that TV shows and even live broadcasts of football matches were replays [17].

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DEJA VU

MAPPING THE MENTAL MATRIX Despite similarities in déjà vu experiences between individuals with and without epilepsy, there are structural differences in the brains of the two populations [9,18,19]. People with TLE who experience pathological déjà vu demonstrate contrasting temporal lobe structures to those without TLE who experience déjà vu [9, 18, 19]. Structural differences in brain tissues are specifically observed in grey matter, the tissue that contains the cell bodies of neurons. Grey matter is crucial for memory processing and the retrieval of episodic memories [18, 20].

Memory processing can be impaired when less grey matter is found in the limbic system, which is a series of interconnected brain regions in the temporal lobe that are involved in the regulation of emotional responses [21, 22, 23]. Emotion plays a large role in the recollection of memories, and since many episodic memories have an emotional aspect to them, the limbic system is strongly associated with the recall of memory and experience of the dreamy state during déjà vu [24, 23]. The structural differences in the brains of TLE patients reveal that TLE-induced déjà vu is fundamentally different from the déjà vu most people experience [21, 22, 23].

The differences between pathological and non-pathological déjà vu are also evident in case studies of individuals who experience both déjà vu forms. In one case of an individual with TLE, déjà vu was experienced both during a seizure and in the absence of a seizure [13]. The person felt a difference between the two kinds of déjà vu; when experienced in tandem with a seizure, it was associated with fear, dysphoria, and worry, whereas non-pathological déjà vu elicited more neutral feelings. In another

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study, a man with TLE tried to minimize his sense of déjà vu by diverting attention away from his déjà vu trigger, but the feeling of familiarity persisted regardless [25]. TLE déjà vu may be caused by more than just a person’s environment and familiarity; however, additional research is necessary [25]. These case studies utilizing self-report measures provide a lens into an individual’s experience, but they may not be generalizable to the broader population.

CONCLUSION Déjà vu inexplicably breaks the rules of our cognitive worlds. It bends what is ‘allowed’ in our memory and what is not. We feel familiarity from a situation we’ve never experienced, and we see the past in the present. Based on the current state of research, the temporal lobe, déjà vu, and dreamy state are interrelated. From errors in memory to differences in temporal lobe structures, there are many different explanations for the universally perplexing cognitive illusion of déjà vu. While the ‘dreamy state’ is specific to TLE, its similarities to déjà vu are strong enough to provide insight into the broader phenomenon. Since the neurological mechanisms of déjà vu have revealed its connection to TLE, we have begun to untangle the complexities and bridges between memory, cognition, consciousness involved in déjà vu. While déjà vu is a fleeting experience and you may not even remember the last time you had it, the sensation is all-consuming in the moment. At its core, déjà vu perfectly symbolizes the brilliant mystery that is the human mind.

It’s a real-life glitch in your matrix.

References on page 54.

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POSTPARTUM DEPRESSION

Beyond Baby Blues: Unpacking Postpartum Depression This article sometimes uses female-gendered language to refer to pregnant and postpartum people. This choice was made because cited literature on the subject frequently focuses on only female-identifying patients. The journal wishes to recognize that pregnancy is independent of gender identity.

by Jack Matter/ art by Laurel Obermueller “The storm hit right away. I was plagued with irrational thoughts and crippling guilt.

I was afraid to show my new baby any affection in front of my toddler for fear that she would think I didn’t love her anymore. I was so depressed that I could not take care of the children” [1].

This is just one of thousands of stories of the turmoil that can take over a mother’s life in the weeks directly after giving birth. This period, known as the postpartum period, lasts anywhere from four weeks to six months and is rife with hormonal fluctuations and waves of strong emotions that last until the body has returned to its pre-pregnancy state [2, 3, 4, 5]. For new mothers, the experience of giving birth can bring profound feelings of joy and attachment. But what happens when this is not the case? Sometimes, the emotional fluctuations associated with the postpartum period can manifest as sadness in a phenomenon typically called the ‘baby blues’ [6, 7, 8].

When this melancholy extends beyond minor mood changes, mothers may be suffering from a specific type of depression known as postpartum depression (PPD) [9].

WHAT IS POSTPARTUM DEPRESSION? What makes postpartum depression different from other depressive disorders, such as major depressive disorder (MDD), is the specific term ‘postpartum’ [10]. MDD is a very common

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POSTPARTUM DEPRESSION psychiatric disorder characterized by a persistent depressed mood [11,12]. While MDD can appear at any point in a person’s life, PPD applies to a major depressive disorder that emerges after a mother gives birth. Psychiatric screening tools like diagnostic manuals are able to detect and diagnose major depressive episodes in the postpartum period as well as differentiate depressive disorders like PPD and MDD from other disorders [10]. Although they are two distinct disorders, PPD and MDD episodes both commonly manifest as persistent feelings of sadness, anxiety, fatigue, and even thoughts of self-harm and suicide [13, 14]. PPD can also involve thoughts of infanticide, or harming one’s own child [15].

Depressive symptoms make caring for a newborn, an already difficult undertaking, significantly more difficult for new mothers. Suicidal ideation and thoughts of infanticide can be overwhelming and can severely impact the well-being of both the parent and the child [16]. Moreover, PPD negatively affects not only a mother and child’s life expectancy but also the growth and psychological development of the child during the postpartum period [17]. Infants with depressed mothers, for example, have a higher chance of being underweight during the first year of their lives, as a depressed parent may struggle to care for themselves and their child [18]. Evidently, PPD can have devastating effects on the entire family, not necessarily just on the parent experiencing the disorder [18].

For a disorder that can have such devastating effects on afflicted individuals and their families, PPD affects a surprisingly significant percentage of new mothers around the world. PPD occurs in around one out of every eight women globally, with some local variations in prevalence due to social stigma, lack of awareness, and medical racism [19, 20]. It is im-

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perative to be mindful of overlapping determinants of health when discussing the risk factors of PPD since several biological and social factors are believed to be responsible for the development of the disorder. In particular, complications during pregnancy, birth, or the postpartum period — including hormonal changes, difficulties with breastfeeding, and whether an infant was born preterm — can increase the likelihood of developing PPD [21]. Additionally, there are correlations between a mother’s degree of bodily autonomy during the birthing experience and the occurrence of PPD [22]. Traumatic birth experiences — such as emergency C-sections or being put under general anesthesia during or after giving birth — can contribute to the development of postpartum disorders [23]. One mother experiencing PPD describes her feelings after she was put under anesthesia by doctors due to birthing complications:

“I can barely remember what exactly happened the first twenty-four hours of my child’s life. Now I constantly fear that me and her missed our connection, or she felt connected to someone more than me who held her when she was first born” [1].

With that being said, the list of possible causes of PPD remains incomplete and some people have developed the disorder without any known or apparent risk factors.

Moreover, PPD is both clinically and experimentally understudied and underdiagnosed [24]. Historically, the research surrounding PPD has failed to accurately represent a broad spectrum of people who experience the disorder or convey how racial factors can affect the individual experiences of mothers with PPD. More recently, scientific literature has begun to address the effects of structural racism on pregnant people [25].

Stereotypes and prejudices surrounding race, ethnicity, and culture can form insurmountable barriers to the timely diagnosis and treatment of mothers of color experiencing PPD [26]. In addition to general stigmas that exist within these communities, there are several intersecting factors that affect PPD treatment and diagnosis. These factors can heighten feelings of isolation and a reluctance to seek help for the disorder [25]. Mothers of color are less likely to receive a diagnosis of PPD and are more likely to experience treatment delays than white mothers [27, 28]. Societal prejudices and stereotypes contribute to the risk of developing psychiatric disorders due to the

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POSTPARTUM DEPRESSION compounded effects of life stressors and decreased quality of care [26, 27, 28].

THE NEUROLOGICAL NATURE OF POSTPARTUM DEPRESSION PPD cannot be researched in standard ways because of the complex ethics of studying pregnant and postpartum people; thus, many aspects of PPD remain a mystery [29]. What we do know about the disorder comes from the use of low-risk functional magnetic resonance imaging (fMRI).

When a person receives an fMRI scan, magnets and radio waves are used to generate an intricate map of their brain activity by measuring blood flow and electrical transmission [30, 31].

These fMRI-generated images indicate that there are both chemical and structural differences in the brains of mothers with PPD when compared to mothers without PPD [32].

One chemical factor implicated in the development of PPD is the chemical messenger glutamate, one of the brain’s primary excitatory chemical messengers. Glutamate has long been known to play an important role in learning, mood regulation, and memory [33, 34]. It is helpful to imagine glutamate as a traffic light for the brain; just as a green light allows cars to move through an intersection, glutamate acts as a ‘go’ signal that prompts cells in the brain to communicate with one another [33]. Moreover, abnormalities in the neurological systems that glutamate is involved in have been linked to depressive disorders [35]. That being said, the specific mechanisms behind these abnormalities are not entirely understood, and their role in PPD warrants further research [36]. One major hypothesis is that the dysregulation of glutamate signaling in PPD relates to changes in the levels of female reproductive hormones [37, 38]. Glutamate levels in the brain increase during pregnancy to support the growth of the fetus, especially during the second and third trimesters [39, 40].

After childbirth, there is a massive, sudden drop in reproductive hormones accompanied by an imbalance of glutamate and other chemical messengers in specific brain regions [41]. For example, in the medial prefrontal cortex (MPFC), a brain region that regulates emotions and memory, levels of glutamate are found to be significantly higher for individuals with PPD [42, 43, 44, 45]. In contrast, decreased levels of glutamate have been found in the dorsolateral prefrontal cortex (DLPFC), which is thought to be involved in learning, planning, and auditory processing [46, 47]. In the MPFC and DLPFC, abnormal levels of glutamate can cause disruptions to the flow of traffic in the brain, since both too much and too little glutamate can negatively affect learning, memory and mood regulation [33, 48]. These discoveries show us that there is a theoretically optimal level of glutamate transmission in the MPFC and DLPFC [32, 33]. However, this ideal level is unknown because people rarely get MRI scans when they are not presenting with a disorder, as they can be costly and time-consuming [49]. This — combined with a lack of data on individual differences and glutamate concentrations throughout the brain — has made it hard to determine a healthy baseline level of glutamate signaling.

The brain is thrown into even further disarray by the disruption of signaling highways that lead to other parts of the brain. In particular, the cingulate cortex, amygdala, and MPFC — several connected brain regions — share these highways, often ‘speaking’ to each other to modulate our moods and actions [24, 50, 51].

The cingulate cortex and the amygdala are heavily involved in behavioral responses, emotions, and memory [52, 53]. The amygdala is also linked to mood and depressive disorders [54]. Disruptions in communication between the cingulate cortex, amygdala, and MPFC regions can potentially impact the emotional state of people with PPD, diminishing mothers’ ability to recognize and respond to their child’s emotional cues [51, 55]. Appropriate emotional response from mothers to cues from their children are vital in

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POSTPARTUM DEPRESSION developing the attachment between mother and child [56]. For example, a major sensory cue that has been linked to maternal depression is sound. Brain scans of mothers with and without depression revealed that non-depressed mothers had increased neural responses to their infant’s cries when compared to depressed mothers [57]. This could mean that the brains of non-depressed mothers are more responsive to their infant’s cries than those of depressed mothers, suggesting that depression in mothers affects their ability to respond appropriately to their child’s needs. The very same networks that are involved in PPD’s symptoms are also involved in a parent’s response to cues from their child, emphasizing how neurological causes aside from glutamate imbalances may play a role in the development of PPD [57].

TREATING POSTPARTUM DEPRESSION HOLISTICALLY Early diagnosis and intervention are crucial for the successful management of PPD [13]. After diagnosis, interventions include both the use of pharmaceuticals and non-pharmaceutical treatments [13]. So far, all of the drug-based therapies that are used to treat PPD have been adapted from depressive disorder treatments, so no specific drugs have been approved for PPD [58]. This means that the application of these therapies to PPD comes with its own set of complications. Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressant medications that have been in use for almost 40 years [59, 60]. They are an effective treatment for major depressive disorders and a strong first line of defense against PPD [59, 60]. Still, these traditionally prescribed antidepressants present certain risks [61, 62, 63]. The use of SSRIs during pregnancy has sometimes been linked to physiological problems in newborns, such as low birth weight and increased risk of respiratory distress [61, 62, 63]. However, some trials resulted in few complications and have found SSRIs to be effective in mitigating symptoms of PPD. The lack of systematic clinical trials studying the efficacy of SSRIs in fighting PPD highlights the conflicting nature of our current knowledge regarding antidepressant use during and after pregnancy [64]. Therefore, antidepressants like SSRIs must be further explored before their efficacy in PPD treatment can be confirmed [65]. The question of whether to start or continue taking antidepressants during

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pregnancy is a challenging one that forces many pregnant people and their doctors to weigh the potentially enormous costs of the drugs against their benefits [66].

Often used in conjunction with medications, nonpharmacological treatments for PPD include psychotherapy, parenting classes, dietary supplements, and physical exercise [13]. One particular type of psychotherapy called cognitive behavioral therapy (CBT) is frequently used to treat PPD [67]. CBT is a form of talk therapy that endeavors to change negative thinking patterns in patients [68]. Another noteworthy postpartum care strategy that can be used in conjunction with CBT is skin-to-skin contact between mother and child [69].

While it may seem like a simple concept, skin-to-skin contact outside of breastfeeding is rarely encouraged despite its numerous physiological and emotional benefits for both mother and child [70]. The main kind of skin-to-skin contact involves a parent holding their baby against their bare chest in an upright position, similar to how a kangaroo holds its baby in its pouch; as a result, this is called kangaroo care [71]. Kangaroo care is easy to do and has numerous benefits for both mother and child, such as pain relief, sleep quality improvements, and even improved heart rate and breathing rate [72]. Thus, it has been found to be effective in preventing and regulating symptoms of PPD and is particularly useful in combination with other modes of treatment like CBT [13, 73].

POSTPARTUM DEPRESSION’S STRUGGLE FOR RECOGNITION Postpartum neurological conditions have a complicated history in the psychiatric field [74, 75]. For more

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POSTPARTUM DEPRESSION than 150 years, the usefulness of a distinction between postpartum depression from other depressive disorders has been highly contested [74, 75, 76].

‘Postpartum’ as a modifier for depression diagnoses is only a recent addition to psychiatric diagnostic tools [10]. Additionally, current American diagnostic guidelines only recognize pregnancy-related depression up to four weeks after birth [77]. However, we know from previous research that the postpartum period lasts anywhere from four weeks to six months, which is inconsistent with diagnostic criteria [2]. In addition to this lengthy debate, various forms of mass media may have inaccurately represented the realities or science of PPD [78, 79]. The media is a major source of health information for most people and can shape people’s beliefs about health, sickness, and body image [80, 81, 82]. Even in people without PPD, the period after birth is associated with decreased self-esteem, which may put pregnant people in a vulnerable state where they are more likely to be impacted by media portrayals of pregnancy and PPD [83]. This impact is even further complicated when mass media and psychiatrists do not agree on something as basic as the definition of PPD [76]. Some popular online media outlets, like news sites, conflate PPD with other postpartum disorders, painting a confusing picture for readers and revealing the continued lack of a consensus on the details of PPD [79]. Very few prominent mass media sites have presented the disorder in a scientifically accurate and non-sensationalized way [78].

Apart from diagnostic complications and inaccurate media representation, there are other barriers to the diagnosis and treatment of PPD. The popular mythology of the ‘supermom’ puts forth the idea that mothers are independent, all-encompassing providers, which can contribute to social isolation when PPD prevents them from properly caring for or bonding with their baby [84, 85]. This message has been reinforced by PPD treatment guidelines and self-help books alike, which both frequently insist that motherhood should bring happiness and that intervention is necessary if it does not [86]. Mothers have expressed feelings of failure and exasperation

when their reality does not align with the expectations that society has placed upon them [1, 87]. Mothers may even develop an aversion to seeking treatment, a phenomenon called self-stigma [88, 89]. As a result, mothers may be more reluctant to accept help and delay seeking treatment for months or even years [90, 91].

The misrepresentation of PPD is a result of the disconnect that exists between the severity of the disorder and the way in which it is medically treated.

PPD is complex and multifaceted in its symptoms, risk factors, and treatment plans [13]. While the exact causes of PPD are not fully understood, some biological mechanisms potentially contribute to the disorder [29]. One crucial area of study that has emerged from PPD research is the role of glutamate imbalance and structural connectivity differences in regulating a person’s emotions and memory [35, 43]. This abnormality in glutamate signaling can disrupt the flow of communication between brain regions, impacting emotional states, memory, and mood regulation, as well as affecting the attachment between mothers and their children [24]. Discoveries like this have advanced our understanding of the brain and its unique inner workings within the postpartum period. As a result, we have a better grasp of PPD and what makes it scientifically distinct from other depressive disorders [92]. Social factors play a critical role in risk factors for PPD, since those with socioeconomic disadvantages and marginalized identities are more likely to face disparities in diagnosis and treatment. When it comes to improving the well-being of those affected by PPD, there are two main areas to focus on. One is promoting general awareness of postpartum depression and improving the accessibility of treatment options like skin-to-skin contact. The other is breaking down barriers that prevent members of marginalized groups from receiving the same level of care as other people with PPD. This way, every family affected by the disorder has the support they need to thrive.

References on page 56.

If you or someone you know is experiencing symptoms similar to those described in this article, know that you are not alone. Help is available at the following resources: Mental health crisis line (US): 988 HRSA maternal mental health line (US): 1-833-943-5746 (1-833-9-HELP4MOMS)

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POSTPARTUM DEPRESSION

A Wrinkle in the Mind: How Prions Infect the Brain

by Sufana Noorwez art by Iris Li 38

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PRIONS t was an average December in MT’s household.

Igetting She was shopping, meeting up with her family, and excited for the holidays ahead. The holi-

days passed by uneventfully, but all of a sudden, she started to notice something strange. At first, the symptoms were subtle enough; she found it harder to do some simple math and to complete normal chores. Over time, the symptoms worsened. MT was confused all of the time, her movements became jerky, and her vision started to blur. Her strange new symptoms resembled those of many common neurological diseases, and yet no matter how many tests they ran, her doctors could not pin down a specific cause or diagnosis. As the days passed, MT’s condition continued to decline; she began to have visual hallucinations and delusions, and started to suffer from seizures [1]. At this point, MT’s doctors began to piece together the puzzle: MT had a rare type of infection called a prion disease, and her prognosis was not good. About 70% of the time, death occurs within one year of symptom onset [2].

In MT’s case, the specific disease was called ‘variant Creutzfeldt-Jakob disease,’ the human manifestation of bovine spongiform encephalopathy, more famously known as ‘mad cow disease’ [3]. Prion diseases are rare and unique, but terrifying; they are nearly untreatable and extremely deadly. Unbeknownst to their victims, prions invade the brain and multiply, presenting a fascinating case of what can go wrong when your body betrays you.

FROM PROTEIN TO PRION FROM PROTEIN TO PRION Prion disease can wreak havoc on essential molecules in our bodies called proteins [4, 5]. As the biochemical workhorses of the human body, proteins are responsible for much of the activity within our cells. Proteins facilitate chemical reactions, make up the structure of our tissues, and move materials around our bodies. The structures of proteins must be carefully regulated during their creation because protein structure is inextricably linked to function.

Even the smallest mistake in form can render proteins incapable of partaking in their crucial roles, including building our body’s tissues, protecting against diseases, and sending signals throughout the body. Proteins need to fold into complex, three-dimensional shapes in order to become fully functional. The folded structure of proteins is determined by a series of chemical reactions, with various conditions — such as temperature — kept constant to ensure proper protein folding [4]. Think of protein folding like making an origami boat. If

you have the correct instructions to form the shape of the boat and you make smooth, even creases, your boat will have good form. The boat’s structure ensures that it can carry out its function: floating. If you rush through the folding, making haphazard folds and creases, your origami boat may no longer resemble a real boat. The boat may even sink when you place it in water. Similarly, the structure of proteins and the way that they are folded affects their function [4].

One extreme example of what can happen when proteins fold incorrectly is the development of prion diseases, in which misfolded proteins cause widespread degradation of the brain [5, 6, 7]. The accumulation of misfolded proteins causes cells in the nervous system to gradually become dysfunctional and eventually die, via a process called neurodegeneration. The same process is seen in diseases like Alzheimer’s and Parkinson’s disease [8, 9]. A prion is a misfolded version of a specific protein called PrP, or cellular prion protein, which is present in all human brains [7].

This misfolded protein, called a ‘prion’ or PrPSc, is the pathogenic, infectious version of the normal PrP — meaning that it can cause and spread disease. The misfolding of PrPSc can happen because of a mutation in one’s genetic code, which arises due to either a spontaneous misfolding or exposure to an already misfolded PrPSc [7]. In all of these cases, the genetic code — which provides the instructions for protein folding — is overridden by PrPSc, allowing the misfolded protein form to prevail [10, 11, 12]. This is similar to the instruction manual for folding an origami boat.

Incorrect instructions, resulting in even just one error in a fold, can have drastic effects on the shape and function of the boat.

The real danger with prions lies in their ability to spread their misfolded state to other proteins of the

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PRIONS same type [13, 14, 15]. Most proteins require a ‘blueprint’ from another protein of the same kind in order to initiate their own folding [16, 17]. Therefore, during protein folding, new PrP latch on to their nearest lookalike neighbor and use their structure as a guide for how they should fold. In the case of prions, when there is one PrPSc, PrP uses this misfolded protein as a template, resulting in the misfolding of the new protein as well. This process is a domino effect: the misfolding of one PrP rapidly causes the misfolding of other PrP in the vicinity [13, 18]. When enough PrP are misfolded, sticky clusters of prions, called plaques, are formed in the brain [19].

PLAQUES LAY SIEGE TO THE BRAIN To understand the effects of prion diseases, it’s crucial to understand the protein that the disease affects, PrP. PrP has a variety of important functions within the mammalian brain, such as maintaining the electrical activity of neurons, and facilitating roles in cell signaling, cell adhesion, and the production of new neurons [7, 20, 21]. PrP may also be involved in our sense of smell and the efficiency of signaling between neurons [7, 22, 23, 24]. Despite the varied functions of PrP, the protein does not seem to be necessary for mammalian survival; complete removal of the protein has no apparent effect on health in a rodent model, although it may minorly affect processes involving PrP [7, 20]. As such, the most crucial, deadly symptom of prion diseases is not the loss of function of PrP, but rather the formation of amyloid fibers and plaques within the brain caused by PrPSc [25]. Amyloid fibers are long, fibrous strands of sticky protein clusters that form once PrP misfolds into PrPSc and begins to accumulate. A collection of these fibers is called an amyloid plaque, and are the structures primarily involved in prion disease neurodegeneration [18, 26, 27, 28]. An accumulation of fibers and plaques can have devastating effects on the cells of our brains, causing neuron death [6, 29]. The backlog of misfolded proteins — which the cell has already tried and failed to get rid of — clog up the protein synthesis center of the cell and prevent the synthesis of more essential proteins, leading the cell into a death pathway [6]. Additional ways through which the conversion of PrP to PrPSc can cause neuron death is by degrading the junctions between nerve cells where chemical signals pass between single neurons. When neurons are no longer able to carry out their function by relaying signals, they break down, degrading from one end of the neuron, where signals are passed, to the

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other end, eventually leading to cell death [6, 30]. This mechanism of neuron death is unique to prion diseases; neurons usually start degenerating and then stop transmitting signals [6]. The rapid death of neurons is what leaves behind the brain holes characteristic of prion diseases [6, 31]. Finally, brain swelling — caused by our immune system’s attempts to clean up plaques — also contributes to neurodegeneration [32]. Although there are a variety of small effects PrPSc has on the brain, the death of neurons seems to be the largest contributor to the fatal symptoms individuals with prion disease experience [6]. If signal communication is compromised, one may experience a loss of motor function, as well as the onset of dementia, headaches, and behavioral changes; this is all characteristic of prion diseases [2].

FROM PRION TO PERSON Prion diseases are exceedingly rare, and the average person will never have to worry about contracting one and experiencing its lethal effects [33, 34, 35].

Creutzfeldt-Jakob disease (CJD) — the human version

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PRIONS and saliva [39, 40, 41].

Prion diseases have also been documented to pass from parents to children through genetic inheritance [42]. Two well-known examples of this mode include familial Creutzfeldt-Jakob disease, which exhibits similar symptoms to regular CJD, and fatal familial insomnia, a disease which renders victims unable to sleep and leads to their mental and physical deterioration [10, 43]. Because PrP proteins misfold into PrPSc due to a faulty genetic code, children can inherit this faulty code from their parents, which makes them susceptible to the prion disease as well. Because prion diseases can lay dormant for years before affected individuals notice any symptoms, people may not be aware of their infection until late in life [44, 45]. Prion diseases can also be spread through medical contamination [46, 47, 48]. When PrP misfolds into PrPSc, it folds into a very stable structure that cannot be degraded by the immune system; it also tends to attract other PrPSc [49]. This stability means that when medical instruments — such as those used in brain surgery or other hospital settings — come into contact with prion-infected tissue, they cannot be decontaminated with standard protocols, which normally clean off any bacteria or viruses [46]. Consequently, prion transmission can occur in hospital settings through surgical equipment and blood transfusions [45].

of mad cow disease — is the most common human prion disease, and was only detected in about one in a million people in the United States between the years of 1979 and 2006 [33]. To put this in perspective, your chances of dying in a car accident are 10,000 times higher than dying from a prion disease, or about one in a hundred [36]. However, prion diseases are still devastating for the unlucky few that encounter them. In order to understand how prion diseases work, we have to understand how they are transmitted. As the name ‘mad cow disease’ suggests, many prion diseases originate from animals.

In the 1980s, an outbreak of ‘mad cow disease’ in the United Kingdom led to the diagnosis of over 100 cases of CJD by 2006 [12]. Infection likely occurred via the consumption of contaminated beef, particularly cuts of meat that contained nervous system tissue, where infectious prion proteins are most highly concentrated [37]. Cattle are not the only culprits either, as prion diseases have been documented in sheep, goats, deer, cats, and even primates [38]. Prions are highly transmissible in animals, and transmission can occur through contact with feces, urine, blood,

In the rarest of cases, prion diseases have been passed from human-to-human through cannibalism [50]. In the case of the Indigenous Fore tribe in Papua New Guinea, ritual cannibalism was a common religious practice intended to free the spirits of deceased tribal members [51]. The Fore tribe also suffered disproportionately from symptoms commonly associated with neurodegenerative diseases — symptoms we now know are because of a prion disease transmitted to tribe members via consumption of the brains of deceased tribe members [52]. This disease came to be known as Kuru, which is the Fore word for ‘shiver,’ as well as a fitting name for one of the hallmark symptoms of the condition: shivering [53]. Once the prion disease impacting the Fore was identified as the cause of the aforementioned symptoms, the tribe worked to decrease the incidence of ritual cannibalism as a mortuary practice in order to decrease the spread of Kuru [50].

DIFFERENT MECHANISMS, SIMILAR OUTCOMES: PRIONS, ALZHEIMER’S, AND PARKINSON’S As mentioned earlier, one unique characteristic of prion diseases is their similarity to other

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PRIONS first two are not transmissible between individuals, while they are transmissible between individuals in the case of prion diseases.

A STICKY END

neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease. The amyloid fibers and subsequent amyloid plaques caused by prion diseases are similar to the same fibers and plaques characteristic of Alzheimer’s disease [54]. Amyloid fibers build up to form sticky plaques that inhibit brain function. This is similar to spilling orange juice all over the keyboard of your computer; the juice makes the keys sticky, rendering them less useful. Because structures formed in the case of both degenerative and prion diseases are so similar, the symptoms experienced by people who suffer from prion diseases and Alzheimer’s or Parkinson’s are also similar. Some of these symptoms include dementia, loss of motor control, insomnia, and behavioral changes [55, 56, 57, 58]. One major difference between Alzheimer’s and Parkinson’s disease and prion diseases is that the causative agents for the

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Much is still unknown about prion diseases, their mechanisms, and the full range of their effects [6].

This may be due to their rarity. While there are currently no approved treatments or prevention strategies for any prion diseases, research is still ongoing [34]. In fact, some decontamination strategies have been developed, primarily involving high temperatures or pressures, which aims to remove infectious protein particles from medical instruments [59]. Additionally, to avoid the fate of those who were accidentally infected after consuming nervous system tissue, it is important to avoid consuming meat that may contain infectious particles [60]. Prion diseases like CJD are extremely rare, but understanding their causes and effects allow for a unique view into the inner workings of proteins, the molecules that make up our bodies and allow us to function. Prion diseases hijack one of the most essential life processes — protein folding — and go on to have remarkable effects on the structure and function of the brain. As their sticky strands accumulate, neurons die and the brain is stripped of its ability to send signals. Without the capacity for communication, quality of life rapidly deteriorates, and prions prevail.

References on page 60.

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ANIMAL NEURO

Exploring the Possibilities of Life Without a Brain

by Sloane Boukobza/ art by Michelle Shaffer A (CAMBRIAN) EXPLOSION CREATED OUR SENSORY SYSTEM

round 541 million years ago, Earth’s terrestriAcalled al surface appeared barren [1]. During this time, the Cambrian Period, large plants and vegeta-

tion had not yet evolved to cover the Earth, and life was small, simple, and squishy. Beneath the ocean’s surface, however, existed a rich and flourishing ecosystem, one which would rapidly evolve in a short period of evolutionary time thanks to one specific creature. This creature, our evolutionary ancestor, was a single-celled, microscopic organism that existed roughly 600 million years ago called the Urchoanozoan [2]. The Urchoanozoan played a foundational role in evolution by allowing for the transition from unicellular microbes to multicellular animals, paving the way for the emergence of complex human sensory systems [3]. The 10 million years following the dawn of multicellular life are referred to as the ‘Cambrian Explosion,’ a period of exponential evolution and diversification among all organisms.

This accelerated diversification resulted in the many forms of life we see today, including most animals.

Despite branching off from each other early on and undergoing separate evolutionary processes, many different types of animals, including humans, independently evolved to share similar traits. Some of these mechanisms, such as the neural structures that are involved in sensory processing, are even more complex in non-human animals than their counterparts in humans. The diversity within animal sensory systems presents alternate pathways and structures which facilitate everyday functions like movement and decision-making. Humans are able to learn from these systems and apply them to technology, expanding the horizons of advancement.

Neural systems have evolved independently in multiple organisms throughout history, which can be seen when comparing at which point in time different animals evolved brains. A human and an octopus both have a brain, yet the emergence of their re-

spective brains is separated on the evolutionary tree by 550 million years, meaning they had no influence on each other’s evolution. This independent evolution of similar neural systems is considered an example of convergent evolution—when two dissimilar species evolve analogous traits to adapt to analogous environmental circumstances. Examining the complexity of neural systems, as well as considering the brain across an evolutionary timeline, serves as an excellent case study in convergent evolution. The brain is a central organ which interprets sensory information,

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ANIMAL NEURO controls body movement, and mediates behavior [4].

Insects, birds, primates, and many marine species all possess complex brain structures despite having various levels of cellular complexity [5]. None of the aforementioned animals share a recent common ancestor with a brain, yet today they all possess this structure that effectively functions as a nervous system control center. Although humans are typically thought of as having the most developed nervous system, many other evolutionarily divergent animals also feature advanced systems; these systems appear to parallel or in some ways surpass those found in humans [6]. By studying the progression of brain structures and nervous systems across animal lineages, scientists are able to uncover the mysteries of life that came before us while simultaneously pushing the boundaries of neuroscience.

BRAINLESS TO BOUNDLESS: THE SPECTRUM OF NEURAL SYSTEMS Around 750 to 600 million years ago, the group Cnidaria—including jellyfish, sea anemones, and coral— split apart from the group Bilateria, a classification which includes most other present-day animals [7].

After the split, Cnidaria and Bilateria evolved independently, with Bilateria going on to encompass a wide range of animals, from humans to octopuses [7]. Although cnidarians don’t have a brain, they are widely regarded as the first organisms to have evolved a nervous system, or a system of cells that relays signals throughout the body [8, 4]. The nervous system found in cnidarians is known as a diffuse nervous system, which consists of a net of neurons interconnected throughout the animal’s body. It is this system that allows cells to directly communicate with each other; the nerves receive input from the senses and process motor output in the area where the nerve is located [9]. Many species within Bilateria, including humans, have instead developed a central nervous system (CNS), which processes information differently from the diffuse system. In the CNS, neurons relay information back to one central point within the body where all of the information from individual neurons is then integrated; this point is known as the brain.

Although Cnidaria and Bilateria split from each other eons ago, their two respective nervous systems evolved in parallel to be able to process and trans-

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mit important information. Cnidarians lack the central brain that bilaterians have, yet their nervous systems contain similar components. Because they lack a brain, cnidarians were once underutilized in research on the evolution of complex neural networks of animals over time. Ultimately, however, their networking system has been extremely useful in better understanding the systems of more recently evolved species like humans. Cnidarians possess specific signaling chemicals which relay information throughout their body’s nervous system. Precisely identical signaling chemicals can be found in bilaterian brains, which is incredible proof of convergent evolution. Considering this overlap, the study of cnidarians is crucial in understanding the initial emergence of the nervous system as well as how the nervous system has adapted across different environments and species [10].

Adaptation is neither static nor linear. After Bilateria split from Cnidaria, many within the group developed a centralized nervous system. This structure is thought to have evolved on five to seven other occasions throughout history, including in chordates (like humans), arthropods (like spiders), and molluscs (like octopuses) [11]. On a smaller scale, within the group of molluscs, there are at least three to four cases where independent centralization of the nervous system has been thought to re-evolve. Each independent evolution of a CNS has allowed the respective species to better adapt to its environment and develop capabilities such as memory and learning [5]. Somehow, these independent cases of evolution converged to yield similar structural results within the nervous system, and understanding this from an evolutionary perspective will lend insight into the origin of the human nervous system.

The centralized nervous system of many Bilateria and the diffuse nervous system of many Cnidaria are radically different, yet there are animals which fall somewhere between the two. Cephalopods, like octopuses and the spiral-shelled nautilus, are a part of Bilateria and have a nervous system which features similarities to the structure of the human brain, including the spinal cord, hippocampus, and wrinkly cerebral cortex [12, 7]. Due to its lack of brain, the nautilus represents an intermediate level of centralization, as its system is neither fully diffuse nor centralized. Its neurons are concentrated in major

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ANIMAL NEURO nerve cords: tube-like structures that run throughout its body to relay information. However, these neurons do not report back to a brain as one does not exist [11]. In comparison to other cephalopods, the nautilus’ nervous system seems to be relatively simple—still, it offers insight into the varying brain systems that evolved in one animal group within the same environment.

BLOBS’ AND BRITTLE STARS’ BRAINLESS BEHAVIOR The phrase ‘structure equals function’ is used throughout scientific literature to emphasize the way in which an animal’s physiological structure serves to optimize its function [13]. In the case of analyzing the structure of the brain and the nervous system, it is the complexity of these structures which accounts for its range of functions [14]. The brain, for example, acts as a highly complex system for processing sensory information and facilitating movement [4]. In humans, its function is supported by the structure of one hundred billion neurons, along with around one hundred billion support cells [15].

A variety of non-human organisms can accomplish similar functions to the human brain while lacking this centralized structure, demonstrating alternate interpretations of the phrase ‘structure equals function.’ The brain allows for complex communication and processing throughout the entire nervous system, but what about the organisms in which a brain is not necessary?

A single-celled, neon yellow blob known as slime mold is a great example of a non-animal organism capable of complex information processing. Sharing characteristics with animals, plants, and fungi, this organism is made up of a single cell composed entirely of a network of interconnected tubes [16].

The complexity of this network of tubes within its one-celled ‘body’ has allowed the slime mold to engage in similar memory processing seen within the human hippocampus, a key brain area involved in short-term and long-term memory. By changing the diameter of each tube within its body through contracting and relaxing, the slime mold can ‘remember’ specified locations by analyzing the changing size of its tubes. The slime mold’s capacity for memory lends insight into an alternative method of memory formation [16].

The brittle star is another organism that contains no brain but is able to perform complex decision-making and movement with the help of a decentralized nervous system. Brittle stars are animals similar to

starfish with five twisty, muscular legs for movement, which all communicate by connecting to a central point at the animal’s center. In animals, movement requires proper transmission and processing of sensory information, followed by nerve responses throughout the body which coordinate the body’s moving parts [17]. For example, humans require a centralized nervous system and brain to coordinate complex motor and sensory information [4]. Instead of relaying this information back to the brain, animals like the brittle star with no centralized nervous system divide and process information in order of importance [17]. For example, signals of injury to one of the brittle star’s arms will get relayed first throughout the organism, while signals of harmless plankton brushing past one of the animal’s arms would take a back seat [7]. The brittle star has evolved to have a nerve ring at its center with a nerve net running through each of its arms [7]. Like highways, each nerve net sends sensory information to the nerve ring at the center. This central ring acts as a roundabout by receiving and redirecting this information, which will be redistributed to highways running through the other arms of the star. This system allows each arm on the brittle star to function as a miniature brain; information essential for survival is sent directly to the nerve ring, while non-essential information is transmitted via the less direct nerve net throughout its body [18]. We see this hierarchical nervous system spring to action when one of the brittle star’s arms has been severed. The animal seemingly allocates the majority of the responsibility for motion to the arms farthest away from the missing appendage, minimizing the restriction of its movement.

Octopuses take it one step further than the brittle star. They demonstrate individualized control of each of their arms, but even when an arm is severed and falls loose, the detached arm can retain its regular behavior [19]. The localized nervous system within the severed arm allows it to continue grasping with its suckers for up to three hours after it detaches [19].

Observing this kind of variation in brain and nervous system functions across animal lineages has allowed us to understand these evolutionarily diverse structures. This creates opportunities for further applications within the human world, where we are limited by the same structure that has allowed us to progress this far: the brain.

NEUROGENESIS - A (R)EVOLUTIONARY HISTORY In the human quest to overcome aging and disease, a roadblock repeatedly presents itself: humans generally do not have the ability to regenerate neurons.

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ANIMAL NEURO The ability to create or regenerate neurons is called neurogenesis, and although this quality is rarely exhibited beyond an organism’s initial development, understanding how it works can directly translate to treating human neurodegenerative diseases such as Alzheimer’s disease [20] When the brain forms in a human fetus, a set number of neuronal cells is generated through a process referred to as embryonic neurogenesis. Only in rare contexts are additional neurons created throughout a human’s lifetime [21].

This means that once a neuron dies, the brain rarely, if ever, produces a new one to replace it. This limitation, however, is not universal throughout the animal world.

Some animals have the ability to generate neurons outside of the initial period of development, a process known as regenerative neurogenesis [22]. The discovery of regenerative neurogenesis played a revolutionary role in our understanding of evolution because neurogenesis was originally thought to halt after birth in all organisms. The starlet sea anemone stands out as a cnidarian known for regenerative neurogenesis [23]. Although this animal cannot perform neurogenesis at all points in its life, this phenomenon occurs as the anemone undergoes a physical transformation from its larval stage to its adult stage, drastically transforming the size and abilities of its body [24]. During this period of transition, the starlet sea anemone is able to direct certain cells to develop into neurons. By modifying its neuron count and composition, the anemone can adapt its nervous system to its new adult life in an aquatic environment [24, 25].

Another creature capable of regenerative neurogenesis is the tobacco hornworm, which modifies its neuron count when undergoing metamorphosis [26]. Similarly to the starlet sea anemone, the hornworm takes on a completely new physical form; it goes further, however, by restructuring its entire CNS. During the hornworm’s transformation into a moth, it utilizes unspecified neuronal cells found in an area of the brain similar to that in humans. The hornworm initiates cell death in obsolete cells in order to make room for these dividing cells, which go on to become functional neurons that will be incorporated throughout the moth’s CNS [26]. Understanding this process has allowed scientists to compare different types of neurogenesis to apply regenerative principles to humans.

Analyzing the growth of new neurons in species with such vastly different evolutionary paths evokes questions about how this information may benefit humans.

The possibility of human regenerative neurogenesis remains alluring because humans are already limited in their capacity for neurogenesis. Specifically, this limited ability is seen within the dentate gyrus of the adult brain, an area of the hippocampus that deals with memory formation [27]. Division of new cells in this area leads to structures that resemble neurons in both form and function, but it is unclear whether these ‘proto-neurons’ are functional [27]. Even though the functionality of these cells remains unknown, their presence within the dentate gyrus allows for improved learning and memory, as well as enhanced neuronal adaptivity over one’s lifetime [28]. This very minimal process of adult hippocampal neurogenesis can be applied to neurological diseases where damaged neurons are unable to be replaced. Species that are already capable of neurogenesis developed this trait as a result of the immense genetic diversity that arose during the Cambrian explosion, and understanding these traits—whether in humans or tobacco hornworms—contributes to the long-term progression of research.

CONCLUSION What if we, as humans, started modeling our research and technology after the organisms which evolved convergently alongside us instead of solely focusing on the structure and function of our own neural system? Every insect, squirrel, bird, and human can be traced back to the Urchoanozoan, a microscopic unicellular organism which lived before the Cambrian period. Within this timespan, animals evolved structures which suited their individual needs, yet an overarching pattern appeared. From nerve nets to cords to rings to a brain, independently evolved neural

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ANIMAL NEURO structures demonstrate repeated evidence of convergent evolution.

It is the differences between these neural systems that ignite scientific innovation. Brittle stars have the ability to redistribute roles across their arms when one is injured based on a hierarchy of priority, which is incredible considering their lack of a centralized nervous system. Octopuses have tentacles which respond in the exact same way, whether their arms are severed or attached to their body. These qualities have sparked new technology that is capable of working in harsh environments. Robots that investigate natural disaster sites or explore outer space are now able to endure severe structural damage and continue collecting data by imitating the brittle star’s adaptability [18]. The study of animal sensory systems formally established the field of ‘biomimicry,’ inspiring the invention of adaptive prosthetics controlled by the mind and nervous system [29, 30]. Although animals with brains dominate today’s planet, observing how nervous systems in animals without a brain delegate responsibility allows these organisms to serve as a blueprint for practical, innovative advances in human technology to further our society.

cesses which humans cannot, such as regenerative neurogenesis, which can break scientific boundaries if fully understood. In people with Alzheimer’s disease, the minimal neurogenesis possible in the dentate gyrus is halted, exacerbating the already widespread death of neurons as the disease progresses. Extensive cell death and a lack of neurogenesis contribute to the deficit in learning and memory characteristic of Alzheimer’s [31]. These cognitive and physical deficits are associated with many neurological diseases, including Alzheimer’s disease, and are currently considered incurable. Analyzing the starlet sea anemone and tobacco hornworm’s regenerative neurogenesis allows for an advanced understanding of how an animal is able to repeatedly produce new neurons throughout its lifetime. Using this knowledge, scientists can induce neuron growth in targeted areas as an ideal therapeutic approach to counteract neurological deterioration [32, 33]. Through studying animals with these diversely evolved neural systems, humans become one step closer to understanding the world’s evolutionary past and reaching a hopeful future built upon the natural innovation of the species around us.

References on Page 62.

In addition to having drastic structural differences, certain animals are also capable of completing pro-

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