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November/December 2016

Doctors Metro MetroDoctors THE JOURNAL OF THE TWIN CITIES MEDICAL SOCIETY

Dementia

In This Issue: • • • • •

The Research The Epidemiology Alzheimer’s Resource and Support Systems Luminary of Twin Cities Medicine


I T R U S T C R U TC H F I E L D D E R M ATO LO G Y TO M A K E M E

“Look Good, Feel Great with Beautiful Skin.”

TM

AES

Catherine S., actual patient, model and student.

THET I C

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Photography by Olivia Crutchfield

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CONTENTS VOLUME 18, NO.6 NOVEMBER/DECEMBER 2016

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IN THIS ISSUE

Dementia: Toward a Greater Understanding By Richard R. Sturgeon, M.D.

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PRESIDENT’S MESSAGE

Forget Me Not By Carolyn A. McClain, M.D.

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TCMS IN ACTION

By Sue Schettle, CEO

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DEMENTIA

Learning to live as “Alzheimer’s Marv” By Marvin Lofquist as edited by Karen Peterson

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Colleague Interview: A Conversation with Anne Murray, M.D.

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SPONSORED CONTENT:

Dementias: Neuropathology as a Tool to Unravel Etiology By H. Brent Clark, M.D., Ph.D. •

Dementia in Long-term Care By John W. Mielke M.D., CMD

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SPONSORED CONTENT:

Alzheimer’s Disease: The Future of Diagnosis, Prevention and Treatment By Michael Rosenbloom, M.D.

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Treating Alzheimer’s With a Big Dose of Policy By Soo Borson, M.D., and Patricia Carlson, MPH

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Traumatic Brain Injury as a Risk Factor for Dementia: Where is the Science and What are its Implications? By Jessica Flores, MS2 and Uzma Samadani, M.D., Ph.D.

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ACT Summit 2016 Building Plans to Act on Alzheimer’s

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TCMS Explores Climate Change and Role for Physicians

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The Convenings: Meaningful Conversations About Living and Dying Well

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Senior Physicians Association Career Opportunities

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LUMINARY OF TWIN CITIES MEDICINE

Sanne Dail Jones Magnan, M.D. Page 6 MetroDoctors

The Journal of the Twin Cities Medical Society

November/December 2016

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Doctors Metro MetroDoctors THE JOURNAL OF THE TWIN CITIES MEDICAL SOCIETY

Dementia

In This Issue:

• The Research • The Epidemiology • Alzheimer’s • Resource and Support Systems • Luminary of Twin Cities Medicine

The reality of dementia’s effect on the human brain. Articles begin on page 6.

November/December 2016

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Doctors MetroDoctors THE JOURNAL OF THE TWIN CITIES MEDICAL SOCIETY

Physician Co-editor Peter J. Dehnel, M.D. Physician Co-editor Robert R. Neal, Jr., M.D. Physician Co-editor Marvin S. Segal, M.D. Physician Co-editor Stephanie Misono, M.D. Physician Co-editor Richard R. Sturgeon, M.D. Physician Co-editor Charles G. Terzian, M.D. Medical Student Co-editor Mac Garrett Managing Editor Nancy K. Bauer TCMS CEO Sue A. Schettle Production Manager Sheila A. Hatcher Advertising Representative Erica Nelson Cover Design by Emily Larsen MetroDoctors (ISSN 1526-4262) is published bi-monthly by the Twin Cities Medical Society, 1300 Godward Street NE, Broadway Place West, Suite 2000, Minneapolis, MN 55413. Periodical postage paid at St. Paul, Minnesota. Postmaster: Send address changes to MetroDoctors, Twin Cities Medical Society, 1300 Godward Street NE, Broadway Place West, Suite 2000, Minneapolis, MN 55413. To promote its objectives and services, the Twin Cities Medical Society prints information in MetroDoctors regarding activities and interests of the society. Responsibility is not assumed for opinions expressed or implied in signed articles, and because of the freedom given to contributors, opinions may not necessarily reflect the official position of TCMS. Send letters and other materials for consideration to MetroDoctors, Twin Cities Medical Society, 1300 Godward Street NE, Broadway Place West, Suite 2000, Minneapolis, MN 55413. E-mail: nbauer@metrodoctors.com. For advertising rates and space reservations, contact: Erica Nelson 4084 Jana Ave. NE St. Michael, MN 55376 phone: (763) 497-1778 fax: (763) 497-8810 e-mail: erica@pierreproductions.com

November/December Index to Advertisers Audiology Concepts .........................................28

TCMS Officers

President: Carolyn A. McClain, M.D. President-elect: Matthew A. Hunt, M.D. Secretary: Thomas E. Kottke, M.D. Treasurer: Nicholas J. Meyer, M.D. Past President: Kenneth N. Kephart, M.D. TCMS Executive Staff

Sue A. Schettle, Chief Executive Officer (612) 362-3799; sschettle@metrodoctors.com Nancy K. Bauer, Associate Director, and Managing Editor, MetroDoctors (612) 623-2893; nbauer@metrodoctors.com Karen Peterson, BSN Executive Director, Honoring Choices Minnesota (612) 362-3704; kpeterson@metrodoctors.com

Coldwell Banker Burnet..................................28 Crutchfield Dermatology..................................... Inside Front Cover Entira Family Clinics .......................................30 Fairview Health Services .................................31 Healthcare Billing Resources, Inc. ...............25 HealthPartners Institute ..................................22 Honoring Choices Minnesota ............................ Outside Back Cover Lakeview Clinic .................................................31

Lynn Betzold, Program Coordinator, Honoring Choices Minnesota (612) 362-3703; lbetzold@metrodoctors.com

M Health ............................................................... 8

Annie Krapek, Assistant Project Coordinator Physician Advocacy Network (612) 362-3715; akrapek@metrodoctors.com

Saint Therese......................................................... 2

Helen Nelson, Administrative Assistant, Honoring Choices Minnesota (612) 362-3705; hnelson@metrodoctors.com

St. Cloud VA Medical Center ............................ Inside Back Cover

Pamela Palan, Project Manager, The Covenings (612) 362-3724; ppalin@metrodoctors.com

Physician Advocacy Network ........................10 Scott Heiligman Realtor..................................13

St. David’s Center .............................................27 University of MN School of Nursing .........21 Uptown Dermatology & SkinSpa................25

At SAINT THERESE, our seniors enjoy life. We offer a full continuum of programs and services available in your own home or in one of our community settings. Senior Apartments Assisted Living Memory Care

Wellness Centers & Rehab Transitional Care Hospice/Palliative Care

Home Health Care Skilled Nursing Pastoral Care

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MetroDoctors reserves the right to reject any article or advertising copy not in accordance with editorial policy. Advertisements published in MetroDoctors do not imply endorsement or sponsorship by TCMS. Non-members may subscribe to MetroDoctors at a cost of $15 per year or $3 per issue, if extra copies are available. For subscription information, contact Andrea Farina at (612) 623-2885.

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November/December 2016

life is good MetroDoctors

The Journal of the Twin Cities Medical Society


IN THIS ISSUE...

Dementia: Toward a Greater Understanding

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lzheimer’s disease is the most common cause of dementia, accounting for 60 to 80 percent of cases and affecting 5.3 million individuals. It is the sixth leading cause of death and the only one of the Top 10 causes of death for which there is no treatment, prevention or cure. An estimated 90,000 Minnesotans have the condition. This Dementia issue will inform and assist us in our caregiver roles. It will also be useful in our family and personal self-care now or at some point in the (hopefully distant) future. Adopting the poignant, insightful direction from Marv Lofquist’s essay, “Alzheimer’s Marv,” will enhance our approach to patients, friends and/or family. As this may very well eventually affect us individually, listen to our wise TCMS President Dr. Carolyn McClain’s useful guidance through those potential choppy seas. Our Colleague Interview, Anne Murray, M.D., elucidates the mixed and still not completely understood multiple etiologies of dementia. She calls out the active research involvement by colleagues in our local health systems. Unhappily, she confirms that we do not, as yet, have any effective long-term treatment or prevention. It seems the only worthwhile preventive measure is regular exercise starting no later than middle age. Lace up your sneakers! Brent Clark, M.D. helps clarify a number of neuropathological disorders that result in dementia. He describes Alzheimer’s disease, frontotemporal dementia, and dementia with Lewy bodies. Developing understanding of gene mutations and their apparent effects on the disease process promotes continued ongoing enthusiastic study to understand and hopefully will eventually allow positive intervention. John Mielke, M.D. informs us of additional special consideration taken with afflicted patients in Long Term Care situations. This includes significant effort to engage with families. With a concerted effort using the interdisciplinary team approach, they have reduced the use of antipsychotics for agitation in many nursing homes from 20-25% to fewer than 10%. He shares information regarding healthcare financing changes as a patient progresses from an acute illness to chronic care. Michael Rosenbloom, M.D. describes the relationship between early-stage Alzheimer’s disease and deposition of amyloid By Richard R. Sturgeon, M.D. Member, MetroDoctors Editorial Board

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The Journal of the Twin Cities Medical Society

and tau. This relationship will be critical in shaping diagnostic approaches and clinical trials. He points out that one needs histopathology for definitive diagnosis and in the antemortem state, one can only have “probable Alzheimer’s.” He presents a very complete picture of the current Alzheimer’s diagnostic and classification information. Looking into the future, he expects dementia research conducted in Minnesota and nationwide to make significant progress in diagnosis, prevention and treatment. Soo Borson, M.D. and Patricia Carlson, MPH emphasize the growing challenges to clinicians and health systems related to increasing incidence of age-related neurodegenerative dementias. Our longer living population’s effect on healthcare delivery calls for system and policy reform with a central focus of new federal legislation and Medicare policy. The National Alzheimer’s Plan (“NAPA”), in a series of recommendations by its Advisory Council of researchers, clinicians and policy experts, has articulated strategies for enhancing the productivity of research on basic mechanisms of neurodegenerative disease and development of new biological treatment targets and new therapeutic agents. Jessica Flores, MS2 and Uzma Samadani, M.D. summarize the current ambiguous scientific pathology literature regarding Chronic Traumatic Encephalopathy and dementia associated with traumatic brain injury. It is clear brain injury is absolutely, unquestionably injurious to the brain with complex multifactorial consequence. A single brain injury is unlikely to cause dementia but is associated with potential psychiatric consequence. Our authors suggest useful information sites for caregivers and patients. Several of these toolkits are already in widespread use with some of our health systems. Our Luminary Sanne Dail Jones Magnan, M.D. has positively impacted Minnesota health care delivery. She led Statewide Policy as our Health Commissioner and influenced quality assurance at the grassroots level with her leadership of ICSI. Thank you Dr. Magnan.

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President’s Message

Forget Me Not CAROLYN A. McCLAIN, M.D.

“IT’S TERRIBLE. THE NEIGHBORS HUNG THEIR CHILDREN FROM THE TREE.

You need to do something about it!” Ms. K, a well-dressed, perfectly groomed 79 year old was visibly upset as the paramedics rolled her into the Emergency Center. “You need to call my son Tommy. He will take care of this.” The nurse was settling her into a room and the paramedics pulled me aside to give me her history. This was her third 911 call today about the kids next door. It was true; they were hanging from the tree...on a rope swing. Ms. K had dementia and her family who, based on her neatly set hair and perfect nails, clearly took incredible care of her were unable to convince her that the neighbor children were okay. Her son Tommy, whom she had asked me to call, had died in a motorcycle accident 30 years ago. As a doctor, I have developed a list of things I am thankful I don’t have: scleroderma, lupus, Crohn’s disease, primary biliary cirrhosis, kidney stones, peripheral neuropathy. Then there are the diseases I don’t have yet...: cancer, heart failure, and yes, dementia. As a coping mechanism for the inevitable, I have contingency plans in my head for when I develop one of these diseases. For cancer, it will be journaling and embracing meditation. For heart failure, I will push for oxygen early so I can continue taking walks. But for dementia? So much of who I am is tied up in my ability to think. I’m smart; that is where I get my self-esteem. Who will I be without my ability to solve problems? How would I even implement a contingency plan? I’ve never been one for crossword puzzles (which are supposed to delay dementia) but apparently now there are smart apps that stave off dementia. And sure, I can try to delay the inevitable, but by age 85, 50% of us have dementia. Chances are, I will develop it. There is a great book called Still Alice by Lisa Genova about Alice, an esteemed Harvard professor who develops early onset dementia. Alice copes with her diagnosis by making an ingenious plan to kill herself when she loses the last bit of memory. But ultimately, dementia foils her plan and she can’t remember to do it. So how can I create a contingency plan? After Ms. K felt comfortable, we talked for a while about her son Tommy. She was still certain he was coming. She had just “called him” and he told her he was on his way. Tommy was a lawyer and he had a wild streak. He would try anything: he went hang gliding in Mexico; he had his pilot license; and he had a string of ex-wives. He graduated summa cum laude from the University of Wisconsin and went to Hamline Law School. But more than anything he loved riding his motorcycle. “You will love Tommy,” Ms. K told me. “Everybody does.” Tommy died on his motorcycle 30 years ago but to Ms. K, he is still right here. The brilliant, gorgeous son she raised could walk in the door any minute. Ms. K does not remember the pain of his death, only the joy of his life. And that joy is what she travels with through her dementia. So how do I cope with the inevitable? Prior to becoming a doctor, I thought like Alice, the heroine of Still Alice. If I get dementia, I want out. I don’t want to live like that. But now... I know in 30 years I may not know who the president of the United States is, I may not know if it is summer or winter, or the address of my home. But I will still have the joy of the life I live today, right now, 30 years before. I will still have my older daughter’s Irish dance performance and my younger daughter’s first soccer goal. I will still have my wedding day and my trip to India. By really living this life today — I am making the memories that I will use to live with my dementia. Through the experiences I am creating today, I am creating my contingency plan for my future and I am comforted by the knowledge that I will get to enjoy all of this again. 4

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The Journal of the Twin Cities Medical Society


TCMS IN ACTION SUE A. SCHETTLE, CEO

Senior Physicians Association

Brooks Jackson, M.D., Vice President for Health Sciences and Dean, University of Minnesota Medical School, was the guest speaker at the September 27, 2016 meeting of the Senior Physicians Association. He provided an “Update on the Medical School.” (See related article on page 30.) The calendar of 2017 meeting dates and speakers will be published soon. All physicians age 62 and older are invited to attend! Watch your email for updates or contact the TCMS Office at (612) 623-2885. Cathy Wurzer of MPR, KARE 11 and TPT to Partner with Honoring Choices MN

A unique partnership is forming with Minnesota Public Radio news anchor Cathy Wurzer, KARE 11, Twin Cities Public Television and Honoring Choices Minnesota. In a series of broadcasts on MPR Cathy chronicled the life journey of Bruce Kramer, the former dean of St. Thomas College of Education, who was suffering with ALS. Those stories led to a book co-written by Cathy and Bruce entitled We Know How This Ends. Before Mr. Kramer died he asked Cathy to carry on with his message about living life to the fullest. Our partnership with Cathy includes a series of events we are calling “Convenings” that will be held throughout Minnesota. We hope to inspire more and more people to have advance care planning conversations using Cathy’s presence in the community. MetroDoctors

In addition, we have partnered with KARE 11 to produce six end-of-life care related stories that will air in November/December. We will also work with KARE 11 in early 2017 to hold a one-hour discussion on the topic. Lastly, we are working with Twin Cities Public Television’s ECHO division to engage with multicultural communities on the topic of culturally sensitive end-of-life care conversations. The team at Honoring Choices MN is so excited about the opportunity to partner with major media partners and to bring the level of awareness of this important topic to the masses. (See related article on page 29.) Honoring Choices Minnesota Highlighted on the National Stage

Honoring Choices Minnesota was featured prominently at two recent national conferences, both in September 2016. The Respecting Choices first-ever annual conference was the first venue where Honoring Choices Minnesota was highlighted as a state-wide communitycentric model. The Coalition to Transform Advance Care (C-TAC) offered Honoring Choices the second venue to highlight our work to obtain funding from the Legislature to expand the statewide reach of advance care planning resources. Environmental Health Task Force Begins its Work

TCMS has recently formed an Environmental Health Task Force looking at the impacts of climate change on our local communities. The work is just beginning — stay tuned for additional information. (See related article on page 27.)

The Journal of the Twin Cities Medical Society

TCMS Partners on Prediabetes

Working in partnership with the City of Minneapolis Health Department, Minnesota Department of Health (MDH) and the local Diabetes Prevention Network, TCMS is currently engaged in activities to educate physicians about prediabetes, encourage screening of patients and referral to a diabetes prevention program (DPP). Efforts to date include: a webinar “Turning the Tide — Easy Tools for Clinicians to Prevent Type 2 Diabetes,” which is being produced featuring Drs. Kacey Justesen and Steven Vincent describing the science behind prediabetes and how to successfully refer to a diabetes prevention program. The webinar will be available in November. Targeted Minneapolis clinics will receive an information packet from TCMS and Minneapolis Health Department including a letter explaining how to access the new MDH Diabetes Prevention Call Center, how to access the webinar for their providers, sample patient education and AMA toolkit promotion materials, and a provider guide/infographic to use as a guide for providers to refer their patients to the Diabetes Prevention Connection for DPP classes. Contact Nancy Bauer at TCMS for more information: nbauer@ metrodoctors.com.

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Dementia

Learning to live as “Alzheimer’s Marv”

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n a prior era of infinite wisdom, I was a chemistry professor. I can remember talking to my students about the need to be honestly introspective about one’s intellectual and academic abilities. I would stress the need for them to realistically assess their abilities before embarking on difficult and challenging tasks. In their case, I was specifically addressing their early desire of “wanting to be a premed student,” which I often saw expressed before time had been spent self-reflecting and asking “do my academic skills and abilities match a premed program?” I retired from teaching in 2010, and in 2012 was diagnosed with amnestic Mild Cognitive Impairment due to Alzheimer’s disease. Now, four years into this journey, I frequently find myself challenging myself the same way I challenged my students: with every choice, before selecting what I want, I need to determine if I have the skills and abilities to still be able to do it. It is an ongoing exploration of the interplay of how my cognition can work to compensate for my declining or absent memory. Cognition cannot replace memory, but it can certainly help mitigate the effects of serious short-term memory loss. I try to keep an informal list of what I can and cannot do, both as a form of mental exercise, and also as a gauge to help me keep my physical and social activities in line with my current abilities. Being a retired scientist, I find I have both the time and inclination to study and explore my personal journey with Alzheimer’s. In 2010, I had no feeling or suspicion By Marvin Lofquist As edited by Karen Peterson

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November/December 2016

that I was having serious memory problems. I felt I was still doing a very demanding job, and my memory issues were related to information-overload. After I retired, we moved from Illinois to Minnesota, to be closer to our family. In this totally new environment, I soon realized I was clearly not learning my way around as quickly or as well as my wife was. Once we started having questions about my memory, there was a tentative acknowledgement by me that yes, there was a change, but also a sense (a hope?) that I was still OK. It was almost “Yes, I am having trouble remembering, but no, I don’t have memory problems — I am just stressed — it is a new environment — I’ll get over this.” But I didn’t. It only got worse. Within a year we were discussing my memory concerns with our new doctor, who thankfully respected our judgment and initiated lab work, an MRI, and testing with a neuropsychologist. The results were below what would be expected for

my age and experience, and that led to more tests. After another year, the confirmation of my memory problems led to the diagnosis of MCI — Mild Cognitive Impairment. Initially, I was in denial, and used my cognition to challenge my doctor’s assertion that my memory was as poor as the tests showed. I think I was ready to acknowledge that I had memory problems, but I was slower to internally process the severity of the problem. It took me awhile to sort out the basic separation between memory and understanding, and what still surprises me today is how cognitive I feel. I often express that I have perceived a serious loss of recall (memory), yet retain a robust sense of understanding (cognition), which I can use to some extent to compensate for the loss of memory ability. Knowing and accepting that I have significant memory loss has paved the way for my wife Elaine and me to better understand my limitations, make our plans, and ensure our practices fit more closely with these realities. It is unfortunate, but necessary, that many of my responsibilities are now taken up by Elaine, or have been transferred to others we pay. For example, we now have someone else prepare our taxes instead of me. We recently moved into an apartment to remove the need for me to care for lawn and house. As I accepted the fact that my memory could not be relied on, the scientist in me looked at it as a data storage and retrieval issue — which led me to recognize that what I needed could be thought of as an external hard drive. I quickly honed in on an iPad as a portable memory device which could work well for me. I carry the iPad with me to many places, and it allows me to look up

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my schedule and write notes to myself and generally serve as my portable memory. My personal experience is leading me to be much more cautious in assuming that I can evaluate how self-aware other people may be who are living with a mental illness. It is so easy to slip into a pattern of not including people in a conversation by assuming that they cannot contribute or they will not understand. This is one of the key messages I would like all physicians to understand. I can follow the logic of many discussions, knowing that I may not remember the supporting details and the arguments. It is like saying I can read a novel and understand the story, without implying that I could later write a detailed synopsis of the book. I can still understand things that I may not be able to easily express. I want physicians to understand that no immediate response does not mean that a person with Alzheimer’s does not understand what is being said. No immediate response simply means no immediate response. It may mean that a longer response time is needed. In my own case, I sometimes just have difficulty in responding immediately because I lose my train of thought as I am thinking of my response. I sometimes feel like I need to stop mid-sentence and say “I lost my train of thought” or “can you repeat the question?” No immediate response does not necessarily mean there is no comprehension, or that the conversation should cease. I may have a disease that is taking away my short term memory, but I can still think and express myself. To offset that challenge, another piece of advice I offer to physicians is

MetroDoctors

that shorter sentences help. Any sentence that requires a second breath may be too long. For me, big words are not as daunting as long, complex sentences. Separating choices into two short sentences, at least by cadence, is a big help. However, I certainly do not want anyone to simplify or “dumb down” their vocabulary. Being able to gauge an appropriate level of communication to a specific person should certainly be guided by your knowledge of the person’s prior life and medical history. I have found all of my doctors to be helpful (I would not go back if they were not.) I have been impressed with how supportive they have been and how they project a feeling of empathy and caring for my situation. I have not pursued treatments outside of our medical programs. I am a scientist and would find it hard to think that on my own I could find therapies that are unknown to the medical profession. I am interested in taking part in clinical trials that are testing new therapies. (Now, I would of course prefer to only enroll in ones that are guaranteed to cure my Alzheimer’s, but for some reason those are hard to find.) Currently I am in a 26-month drug study of subjects with amnestic MCI due to Alzheimer ’s disease. Of course, I do not know if I am taking a placebo, the low dose or the high dose of the drug, but, for me, it seemed only natural to want to be involved in a clinical trial. Alzheimer’s is a terrible disease. Until we have a cure, the best way to soften the effects of dementia is through the support of family and friends.

The Journal of the Twin Cities Medical Society

It is the personal connections that sustain my wife and me. The medical professionals, the people at the Alzheimer’s Association, and the many people we have met in various programs have been a great source of information and are a continuing emotional support. I know I am not alone on this journey, and that makes all the difference. I have Alzheimer’s, but Alzheimer’s does not define me. In a way, I had to have a funeral for the old Marv and now learn to live as the new Alzheimer’s Marv. The new Marv is very open with people about the memory loss and what that means for my ability. Both Old Marv and Alzheimer’s Marv cohabit in me, and both are constantly changing. There is certainly a flow over time that brings more of Alzheimer’s Marv, and weakens and reduces the presence of Old Marv. But the lines are not a firm separation, and there is a flow between the two faces of the one Marv. I am still Marv, and that is what matters. Marv is always open to meet with physicians and/or groups about this journey with Alzheimer’s disease. Please contact Karen Peterson, Executive Director, Honoring Choices Minnesota, kpeterson@metrodoctors.com.

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is for Stroke Care.

University of Minnesota Health Stroke Center specialists are leaders in the advancement, treatment and research of innovative cerebrovascular care. Certified as a Comprehensive Stroke Center by the Joint Commission, we are recognized for our expertise in the diagnosis, treatment, recovery and prevention of stroke and cerebrovascular disease. We apply a multidisciplinary and collaborative approach to patient care, from our stroke neurologists, neurosurgeons and neurointerventional specialists, to our physical medicine and rehabilitation specialists, nurses, pharmacists and care coordinators. We also train the next generation of physicians specializing in vascular neurology, neurointerventional radiology and neurosurgery and conduct clinical research to advance the treatment, prevention and recovery of acute stroke. Learn more about our expert, innovative care at mhealth.org/strokecare

The University of Minnesota Health brand represents a collaboration between University of Minnesota Physicians and University of Minnesota Medical Center. Š 2016 University of Minnesota Physicians and University of Minnesota Medical Center


Dementia

Colleague Interview: A Conversation with Anne Murray, M.D.

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nne Murray, M.D. is the Medical Director, Berman Center for Outcomes and Clinical Research at Hennepin County Medical Center. She received her medical degree from the University of Minnesota Medical School; M.Sc. from Harvard School of Public Health (Epidemiology); completed a residency in Internal Medicine at Mayo Graduate School of Medicine; a Fellowship in Geriatrics, Division on Aging at Harvard Medical School, served as a Kellogg Fellow, Harvard University School of Public Health, and a Hartford Foundation Research Fellow. Dr. Murray is a Professor of Medicine, Clinical Scholar Track, University of Minnesota Medical School and a Faculty Member in Gerontology, the Graduate School University of Minnesota. She is a former President and Chair of the West Metro Medical Society (Twin Cities Medical Society).

Is dementia a disease or simply the aging process? Dementia is a disease and is not part of normal aging. About 10% of current adults can expect to develop dementia before their death. The prevalence of dementia increases exponentially with each decade after age 65, to about 10% between ages 6574, 20% ages 75-85, and over 50% for those ages 85 and older.

Please comment on the various forms of dementia — the etiologies, frequency, clinical course implications and as a comorbidity with another condition such as Parkinsonism or chronic kidney disease. Entire textbooks are written regarding dementia, so we’ll stick to the basics. Dementia is the umbrella term for chronic global cognitive impairment that encompasses multiple etiologies. Although it was previously believed that there was usually one primary etiology for a given case of dementia, it is now understood that most cases have three or more pathologies on brain autopsy that contribute to the dementia. This is one of the reasons no clear cure or preventive medication has been identified for dementia: most investigational medications have been targeted to only one brain pathology. Mixed Alzheimer’s disease/Vascular dementia is viewed by many as the most common form of dementia, based on brain autopsy studies in patients with previous cognitive assessments.

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The most common individual cause of dementia is Alzheimer’s disease (AD). The other common primary causes of dementia include Vascular (previously known as multi-infarct), Lewy body disease (most often seen in Parkinson’s disease, but often seen in other dementias), frontotemporal dementias, or tauopathies (including Pick’s disease), and hippocampal sclerosis. Traumatic brain injury, HIV dementia, and Wernicke-Korsakoff ’s (B1 thiamine deficiency due to alcoholism) dementia are other less common causes, as are other neurodegenerative diseases, metabolic and infectious causes and tumors. Age is the strongest risk factor for dementia, and each year of education beyond high school is protective against dementia. Factors that contribute to all types of dementia include the same cardiovascular risk factors that increase the risk of cardiovascular disease: mid-life hypertension and abdominal obesity, chronic inflammation and oxidative stress, diabetes, and lack of exercise, or sedentary behavior. (Elevated lipids are controversial). Diabetes doubles the risk of dementia. Chronic kidney disease (CKD-pre-dialysis) is another more recently described strong risk factor for cognitive impairment. CKD patients have tremendously elevated levels of inflammation, almost all have hypertension and 50% are diabetic. There are about 3 million people in the U.S. with moderate to late stage CKD (most over age 60), defined as a reduced estimated glomerular filtration rate (eGFR) of less than 45 mL/min/1.73 m2. (Continued on page 11)

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Order free copies at www.panmn.org/patient


Colleague Interview (Continued from page 9)

Risk of cognitive impairment increases as eGFR declines overall; as renal function declines, so does cognitive function. An eGFR < 30 increases the risk of dementia-level cognitive impairment by about 80%, and being on hemodialysis more than doubles the risk, based on the work by my research group and others. My group at the Berman Center at HCMC is conducting a longitudinal observational study called the BRINK (BRain IN Kidney disease) study in 575 participants to measure how commonly cognitive impairment occurs in CKD and its risk factors. We’ve found that CKD affects memory as well as executive function, and to a lesser extent verbal skills, and that about 25% of patients with an eGFR < 30 have severe dementia-level cognitive impairment. Our BRINK brain MRIs have shown both macro and microvascular disease and atrophy consistent with AD, but especially decreased white matter tract integrity and increased volumes of white matter hyperintensities. We have also preliminarily identified elevated serum phosphate as a risk factor for cognitive impairment. As elevated phosphate is treatable with affordable oral phosphate binders, it could be a way to prevent cognitive decline in CKD. This study has been funded by the National Institute on Aging. We are currently seeking funding from multiple sources to continue BRINK study follow-up to confirm this and other risk factors for cognitive decline in CKD. AD is the most common primary cause of dementia, accounting for about 70% of cases (depending on population studied). AD is still defined pathologically by the combined presence of amyloid β42 plaques and tau tangles in the brain, especially involving the hippocampus and temporal lobe, but the field is gradually moving away from the assumption that they are the direct causes of AD (the amyloid hypothesis). The plaques and tangles may simply be the ‘scars’ or signs of the pathophysiologic processes that cause the neuronal damage leading to dementia. Instead, the roles of amyloid and tau oligomers and synaptic pathologies are being explored. Dr. Karen Ashe and colleague Dr. Sylvain Lesné are conducting extraordinary research in these areas using mouse models at the N. Bud Grossman Center laboratory at the University of Minnesota. AD is characterized by a gradual inexorable cognitive decline lasting up to 20 years (average about 12-14 years), depending on when the diagnosis was made. Common early symptoms of AD are apathy or social withdrawal, in addition to the well known short-term memory loss and word-finding difficulties. These symptoms characterize the mild cognitive impairment (MCI) phase of AD. Long-term memory is often well-preserved until late stages of AD. Early signs of impaired executive function are often also present, and include the inability to carry out instrumental activities of daily living, such as maintaining financial records, planning an event or travel, or shopping. Driving ability varies, but by mid-stage AD is usually quite impaired due to impaired judgement, delayed reaction time, and loss of navigational skills. Recurrent paranoid delusions, or paraphrenias, e.g. the patient’s spouse is cheating on them or someone is stealing from them,

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may present in the early- to mid-stages of the disease, but usually resolve over 1-2 years. AD progresses in end-stage to complete loss of independence, requiring 24 hour care. “Pure” Vascular dementia is uncommon because there are usually other brain pathologies playing a role; thus the term vascular cognitive impairment is now more often used to describe the vascular component of dementia. Vascular pathologies include small and large infarcts, subcortical infarcts and microvascular arteriosclerosis, which presents in part as periventricular and subcortical white matter hyperintensities on brain MRI, or ‘white matter disease’. Prolonged hypertension is often associated with microvascular pathology. The natural history of vascular dementia was previously characterized by a step-wise or staccato-type pattern of cognitive decline associated with each stroke/TIA episode, followed by a plateau. Although the risk of dementia after a cortical symptomatic stroke is increased twofold, it is generally recognized that cases with several small or large sequential strokes are relatively infrequent. Instead, a more gradual course may be more typical due to subcortical, often asymptomatic infarcts and progression of microvascular pathology. Vascular cognitive impairment has classically been typified by greater impairment in executive function compared to memory loss, and often language (aphasia), but realistically the cognitive domains affected will be related to the areas of the brain affected by vascular pathology. Frontotemporal dementias (FTD) or tauopathies, are characterized by higher density tau tangles in the frontal and temporal lobes. Classic symptoms of FTD are personality changes due to disinhibition of the frontal lobe, such as increased swearing, sexual aggression, other socially inappropriate behaviors and mood swings. Word finding and verbal skills are impaired to a greater extent than memory initially. Onset is often in the 60s and 70s and life expectancy is usually 6-8 years after diagnosis. Lewy body disease/dementia usually occurs in the setting of Parkinson’s disease, but Lewy inclusion bodies are often found as concomitant pathology in other types of dementia. The α-synuclein protein is the primary constituent of Lewy bodies, and α-synuclein oligomers appear to play a strong role in the neuronal damage associated with Lewy body disease. The gene for α-synuclein, called SNCA, also increases the risk of Parkinson’s disease. At least 50% of patients with Parkinson’s disease will develop dementia, although not always Lewy body dementia. Lewy body disease symptoms include memory loss but also visual hallucinations, fluctuating level of alertness and cognitive symptoms, tremors and rigidity. Hippocampal sclerosis is a more recently identified contributor to dementia and is defined as severe neuronal cell loss and gliosis (scarring from dead neurons) in the hippocampus. About 15% or more of cases that were thought to be AD were due to hippocampal sclerosis in one study. Memory loss is the predominant early symptom, but its symptoms may mimic those of AD and FTD.

(Continued on page 12)

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Dementia Colleague Interview (Continued from page 11)

How does Early Onset Alzheimer’s disease differ from the more common occurrence in the elderly? Early onset AD is defined as cases that are diagnosed before age 65. Most patients are diagnosed in their 40s and 50s and have familial AD, with an autosomal dominant inheritance (i.e. a child has a 50% chance of inheriting the gene if one parent had the gene). About 5% of all AD cases are early onset, or about 200,000 cases. Many readers may be familiar with the ongoing NIH-funded clinical trial of a new amyloid antibody, crenezumab, in a large extended Colombian family with early onset AD, led by Eric Reiman M.D. and his group at the Banner Institute in Arizona.

Are there reliable genetic tests to disclose the probability of an asymptomatic young person eventually developing dementia? The APOE genotype on chromosome 19 is the most commonly tested genotype for Alzheimer’s disease. About 20% of the general population carries the APOE ε4 allele, which increases the risk of AD. (The APOE ε2 allele is protective, and the ε3 allele appears to be neutral). Although the ε4 allele increases one’s risk of developing AD, it is still not a reliable predictor of who will get Alzheimer’s disease. Previous studies have shown that even in people diagnosed with AD, up to 30% do not carry an APOE ε4 allele. Thus it is not generally recommended to get APOE genotype testing in an asymptomatic individual without a history of familial AD. However, it is has been shown that having one copy of the ε4 allele increases the risk of AD by about 2-3 fold (depending on whether the other allele is an ε2 or ε3 allele), and 2 copies of the ε4 allele increases the risk up to 15 fold.

When caring for patients with dementia — how should providers handle history-gathering, decisionmaking, informed consent, especially in situations where the patient has limited insight into their own impairment? Providing care for dementia patients is at once challenging and rewarding — I find dementia patients fascinating. However, it is not possible to obtain an accurate history or informed consent for release of information or a research study unless the primary caregivers or an informant are present. It is not advisable for dementia patients to attend a clinic visit without a caregiver or reliable informant, who in some cases may be a nurse from a nursing home or assisted living. Tracking down critical information regarding a new symptom or behavior problems by follow-up phone calls is much less effective and very time consuming, and most clinics don’t have the luxury of a nurse with dedicated time to conduct such phone calls.

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Are there differences in treatment approaches depending upon which type of dementia exists — e.g. Alzheimer’s vs. Atherosclerotic (bilateral lacunar) vs. Frontotemporal? Yes, but the bottom line is that no medication has been identified that is effective in preventing or reversing dementia long-term. Donepezil and memantine are commonly used medications that may slow the symptoms of AD and vascular or combined AD/ Vascular dementia for one to two years. However, there are many ongoing national clinical trials with a broad range of medications and vaccines designed to either prevent or slow cognitive decline and dementia. Nasal insulin may prove beneficial in improving memory and is undergoing clinical trials nationally and here in the Twin Cities. Neurologist Dr. Mike Rosenbloom and Leah Hanson, Ph.D., are leading this study and currently enrolling eligible patients with mild cognitive impairment or early AD at HealthPartners Center for Memory and Aging (651-254-7936). In addition, the ongoing ASPREE (ASPirin in Reducing Events in the Elderly) trial sponsored by the National Institute on Aging, is measuring whether low dose aspirin 100 mg daily vs. placebo may decrease the risk of dementia, disability or death in 19,000 people 70 and older over about five years in the U.S. and Australia. I am the U.S. principal investigator for the ASPREE study, and the Berman Center for Clinical Research and Outcomes at HCMC is the U.S. coordinating center. ASPREE is in its fifth year of follow up, and we estimate the trial will end in 2018. It would be tremendously exciting if it turns out that a low cost simple aspirin a day could decrease the risk of dementia. The most effective lifestyle preventive intervention for everyone however appears to be regular exercise! Exercising including aerobic or strength-training for at least 30 minutes/day has been found to decrease risk of cognitive decline in multiple studies, and in one study regular walking slowed the rate of hippocampal shrinkage. Adhering to a Mediterranean or similar diet also decreases the risk of cognitive impairment. Early lifestyle intervention is key: the most effective time period to decrease or modify risk factors for cognitive decline is in middle age. Such modifiable risk factors include exercise, blood pressure, blood sugar/diabetes, abdominal obesity and a healthy diet. There are currently several ongoing European trials measuring the effect of multiple lifestyle interventions on cognitive decline; e.g., exercise, nutrition and blood pressure management.

What are the benefits of conducting dementia clinical research within the auspices of a facility such as HCMC’s Berman Center for Clinical Research? The Berman Center has a 25-year history of conducting clinical trials (ALLHAT, WHI, ACCORD Memory in Diabetes-MIND studies) and observational studies, and is fortunate to have the strong support of the Minneapolis Medical Research Foundation (MMRF), based at HCMC. We have the tremendous advantage of being located at HCMC with its diverse patient population MetroDoctors

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and senior care clinics to recruit from. More importantly HCMC and Hennepin Health Systems are dedicated to the research mission, and have recently entered a joint agreement with MMRF to provide career development research awards to promising young investigators to ensure the continued growth of our rich research heritage at HCMC.

What are the challenges in developing a Geriatric curriculum for other residents (non-Internal Medicine/Family Medicine) and what is unique in the training for Geriatric fellows? The greatest challenges for non-primary care specialty training is to at least touch on the most critical geriatric topics common to all areas: 1) recognizing the existence of and understanding the impact of subtle and more severe cognitive impairment and frailty on the overall care of patients within each specialty area, including self-care and functional impairment, 2) the ability to follow a prescribed care regimen, 3) medication adherence, and 4) home and community safety. It is possible that each specialty training program may address diseases within their specialty common among the elderly. However, I am not aware of any local non-primary care curriculum that specifically addresses these as high priority areas , other than a new HCMC initiative to develop a cross-specialty physician home-visiting teaching program. The one year Geriatrics fellowship at HCMC integrates these principles and teaching about system improvement within a broad range of geriatric care venues and specialty care areas. We

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have an excellent group of eight Geriatricians and nine Nurse Practitioners that contribute to the fellowsâ&#x20AC;&#x2122; training, led by Drs. Lawrence Kerzner and Abigail Holley. Aspects of our Geriatric fellowship training include working in a team-based approach with nurses, social workers and PharmDs in providing longitudinal and geriatric consultation care of outpatients, nursing home and home care patients, dementia and Geriatric Psychiatry training at the Minneapolis VAMC, a falls prevention clinic, rotations in urinary incontinence with our Urologists, stroke clinic, Parkinsonâ&#x20AC;&#x2122;s and movement disorders at the Struthers Parkinsonâ&#x20AC;&#x2122;s Center, rehabilitation medicine, wound care, sleep disorders, bone metabolism, palliative medicine and biomedical ethics. Fellows participate with community agencies including the Minnesota Visiting Nurse Agency and Hospice of the Twin Cities in providing direct care in patient homes. Additionally, they work with the Hennepin County Vulnerable Adult Protective Service and the Vulnerable Adult Law Enforcement team to provide consultation visits with their social workers to clients in their place of residence, evaluating and advising regarding elder abuse, neglect, financial exploitation and self-neglect, and participation with the Minnesota Elder Justice Center. The totality of these Geriatric medicine educational experiences is unique among the training programs available to physicians and provides Geriatrics fellows with broad skills and perspectives targeted at helping seniors obtain maximal functional ability and independence, and helping them and their families manage illness and decline in the end of life period.

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Dementias: Neuropathology as a Tool to Unravel Etiology Contributed by H. Brent Clark, M.D., Ph.D.

The neuropathological bases of dementia have become better understood during the past several decades. Despite a common misconception that all dementia is secondary to Alzheimer’s disease, there are a number of other pathological forms of dementia. A shared feature of these disorders is the abnormal accumulation of proteins within cells of the nervous system. This article reviews the neuropathology and possible etiologies of the three most common neurodegenerative dementias: Alzheimer’s disease, frontotemporal dementia, and dementia with Lewy bodies. These conditions typically are sporadic, but study of rarer inherited forms has led to insights into their etiologies. Alzheimer’s Disease

The most common type of dementia, Alzheimer’s disease (AD), typically presents as problems with memory, including difficulties with spatial memory and memory formation. As the disease progresses, patients experience a global loss of cognitive function. The disease is characterized by the presence of neurofibrillary tangles, cytoplasmic accumulations of an inappropriately phosphorylated form of a protein called tau. The second histological hallmark is the presence of senile plaques, extracellular accumulations of a peptide called A-beta, often in an amyloid configuration, that is intermingled with abnormally dilated neuronal processes (Figure A). Neurofibrillary tangles and neuronal loss first occur in the mesial temporal lobes, areas of the brain associated with memory formation, which explains 14

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the early clinical features. The role of the plaques and tangles in the pathophysiology of the disease is not clear, and there is no strong correlation between severity of dementia and severity of plaque deposition. The spread of tangles beyond the mesial temporal zones as the disease progresses correlates better with cognitive disability, but other pathological changes — such as somatic and dendritic atrophy, synaptic loss, and neuronal death — also are critical elements of the pathology. Our growing understanding of genetic mutations associated with AD has led to a better understanding of its etiology. Three autosomal dominant mutations causative for AD have been identified. One occurs in the gene for the amyloid precursor protein (APP), which is the larger protein from which the A-beta peptide, a 40-42 amino acid segment, is cleaved. The most common mutation is in presenilin-1, a protein involved in the processing of APP, which is a function shared by the other

Figure A. Silver stain showing neurofibrillary tangles (on left) and senile plaques (on right) associated with Alzheimer’s disease.

known target for mutation, presenilin-2. Another genetic factor, a variant in apolipoprotein E, the epsilon 4 allele, while not causative, increases the risk for AD by as much as twelvefold if present in the homozygous state. Its role in the pathogenesis of AD may relate to its effect on processing of A-beta. It appears that APP and A-beta have a critical role in the initiation of the disease process. The A-beta in senile plaques often takes the conformational form of amyloid, but because the amyloid burden does not correlate well with degree of dementia, many investigators believe that monomers or oligomeric aggregates of this peptide are toxic to neurons and may be a major pathogenetic factor. Other contributory factors to the pathogenesis of AD include microglial activation. A form of neuroinflammation, microglial activation once was thought to be only a secondary reaction to neurodegeneration, but is now considered a likely contributor to pathogenesis. These inflammatory changes may be accompanied by oxidative stress and mitochondrial dysfunction. Concomitant cerebrovascular disease of any type increases the risk of dementia, even with lower burdens of tangles and plaques. Diabetes mellitus also increases the risk of AD. The greatest risk factor, however, is age, with AD’s

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prevalence reaching nearly 50% among those ages 85 and older. Frontotemporal Dementia

A rarer form of dementia, frontotemporal dementia (FTD), was in the past commonly known as Pick’s disease, a term now restricted to a distinctive subtype of FTD. Until the past two decades, FTD was identified solely by the distribution of atrophy in the frontal and temporal lobes, with the rest of the brain less affected. Clinical manifestations of FTD are more variable than in AD and appear in two basic patterns. The “behavioral” pattern, often initially mistaken for signs of psychiatric disease, is characterized by disinhibition, loss of social graces, apathy, and deficits of executive functions, with memory and visualspatial functions spared in the early stages. The “primary progressive aphasia” pattern includes variable problems with semantic memory, expressive aphasia, or slow nonfluent speech and poor comprehension. Studies of the dominantly inherited forms of FTD have identified genetic mutations associated with FTD and increased our understanding of its pathogenesis. Mutations in the gene for tau, the same protein seen in neurofibrillary tangles, account for some cases of FTD. These patients accumulate abnormally phosphorylated tau in their brains, largely in glial cells. Pick’s disease, although a sporadic form, also is characterized by tau-containing neuronal inclusions (Pick bodies). More recently, studies of other FTD-kindreds have found mutations in the gene for progranulin, a protein involved in regulation of inflammation. Patients from these families have abnormal intranuclear neuronal aggregates of a protein called TDP-43, a RNA/DNA-binding protein normally involved in regulation of gene transcription. When brain tissue from patients with sporadic FTD has been examined for TDP-43 immunoreactivity, this nuclear protein has been found to be abnormally translocated from the nucleus to the cytoplasm of some neurons (Figure B). More recently, an additional mutation has been found in a gene on chromosome 9 (C9orf72). The mutation is an expansion of a hexanucleotide repeat, GGGGCC. One hypothesis is that messenger-RNA MetroDoctors

Figure B. Frontotemporal dementia with cytoplasmic inclusions immunostained for TDP-43 (brown foci).

containing the expanded abnormal repeat sequesters certain transcriptional splicing factors and causes alterations in proteinexpression patterns. There also is evidence that a novel mechanism of protein translation across these expanded repeats results in the formation of dipeptide-repeat proteins that accumulate in cytoplasmic inclusions within neurons and could contribute to pathogenesis. Abnormalities of TDP-43 and mutations in C9orf72 also have been identified in many patients with amyotrophic lateral sclerosis (ALS), suggesting a link between that condition and FTD. Dementia With Lewy Bodies

Lewy bodies, intracytoplasmic neuronal inclusions composed of the protein alphasynuclein (Figure C), are associated with another form of dementia. They also are the characteristic finding in idiopathic Parkinson’s disease. Many patients with Parkinson’s disease develop cognitive problems, but in some patients the dementia precedes the onset of the movement disorder by at least one year. That presentation is termed dementia with Lewy bodies (DLB), but pathologically the two often are indistinguishable at end stage. The

Figure C. Cortical neuron containing a Lewy body.

The Journal of the Twin Cities Medical Society

clinical features of DLB differ from AD in that memory loss is not the predominant presenting feature, although it may develop later. Deficits in executive function, attention, and visual-spatial abilities are often seen at onset. Visual hallucinations also are a characteristic feature, as is diurnal or day-to-day fluctuation in cognitive impairment. Even in patients who present initially with dementia, Parkinsonian features usually develop. Involvement of the cerebral cortex and limbic areas tends to correlate with cognitive changes in both patients with Parkinson’s disease-related dementia and DLB. At autopsy, the characteristic pathological changes in patients with DLB are widespread, and it is difficult to determine whether dementia preceded or followed the onset of Parkinsonism. To further complicate matters, there is a significant crossover of AD-related pathology in patients with Parkinson’s disease and/or DLB. A number of genetic mutations have been associated with DLB/Parkinson’s disease. Of interest, one of those mutations is in alpha-synuclein, the principal component of Lewy bodies. Other mutations are in proteins involved in protein and lipid metabolism, mitochondrial function, and immune mechanisms. Regardless of the underlying mechanism, DLB is characterized by an intraneuronal accumulation of alpha-synuclein, which particularly when in oligomeric forms, may be harmful. Lewy bodies could represent a compensatory attempt to sequester the toxic protein into less harmful large aggregates. A recent hypothesis proposes that the spread of the disease within the nervous system is mediated via trans-synaptic passage of abnormal conformational forms of alphasynuclein in a manner similar to what is thought to occur in prion diseases, such as Creutzfeldt-Jakob disease. Dr. H. Brent Clark is the director of neuropathology at the University of Minnesota Medical School and University of Minnesota Health and is a professor in the Departments of Laboratory Medicine and Pathology, Neurology, and Neurosurgery. He has had a longstanding interest in the pathology of neurodegenerative diseases, particularly the hereditary cerebellar ataxias. November/December 2016

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Dementia

Dementia in Long-term Care

“We have only one choice to make, we should make it!” (so says the wizard Gandalf in the movie version of The Fellowship of the Ring by J.R.R. Tolkien). The wisdom of that statement is founded in an undeniable reality (the gates have collapsed behind them forcing a trek into the mines of Moria). Practically, that “choice” acknowledges that there is no going back — The Fellowship must move forward. Dementia in long-term care (LTC) is quite similar. The diagnosis of dementia is a collapse of any sense of “returning to the way things were.” The way forward is dark and unknown, leading to an intense desire to “get back home — to normal.” But there is no going back to normal. It often falls to the transitional care or LTC team to convey that difficult message, “You have only one choice to make, live with dementia, and now we need to make many decisions!” It is, after all, a “Fellowship of the Ring” moment; we are in this together, and we will get through it together. Communication Between Medical Teams

The new diagnosis of dementia often follows an incident hospitalization for a fall, medication non-compliance, or medical complications as a result of failing cognition. Post-op delirium and “behaviors” in the hospitalized patient are often the early clues to the severity of dementia that has been unnoticed or minimized by family members and the patient. The simple process of admission and discharge from home to hospital to transitional care is enough to exacerbate previously unrecognized cognitive losses. By John W. Mielke M.D., CMD

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Family Expectations

There is a natural tension between hospitals needing to discharge in a timely fashion and nursing homes accepting patients that they can reasonably manage. At times this has led to less than full disclosure about the nature of cognitive losses, leading to inappropriate placement (e.g. assisted living vs. assisted living memory care). Families may perpetuate this miscommunication due to financial constraints* (see sidebar) or denial of the underlying condition. Ultimately, this is counterproductive. This leads to the excessive use of sedatives and antipsychotic medications and re-hospitalizations. Effective communication, on the other hand, leads to effective care planning, developed pre-transfer. There are special accommodations for rehabilitation of the delirious and demented resident: private rooms; rooms closer to the nursing station; non-pharmacologic interventions and careful medication reconciliation can all be beneficial in successfully transferring a dementia resident into a transitional care/skilled nursing care setting.

Families are becoming increasingly sophisticated in their approach to medical care for their elders and, as a result, have higher expectations of our care. Often, they are in denial about the nature and extent of cognitive losses in their elders. This creates significant tension at all levels of the care spectrum: from independent living housing advisors to the transitional care team. In the transitional care setting we have the opportunity to study the elder’s cognition over time. We can allow the delirium to clear, adjust sedating medications, discontinue anticholinergics and antipsychotics and use time to heal. The collection of objective data is very helpful in making clearheaded choices about discharge. Communication between family and providers can elicit previous clues to cognitive losses — inability to balance the checkbook or buy groceries, lack of selfcare, etc. These are valuable assessments for future decision-making concerning living situations and the amount of inhome care needed. The screening tests are used: SLUMS (St. Louis University Mental Status, MOCA (Montreal Cognitive Assessment), MMSE (Mini Mental Status Examination). The PHQ9 is administered by social service to assess for depression. Based on the screening tests, more indepth testing is done by an Occupational Therapist or Speech Language Practitioner: Allen Cognitive Levels (ACL) or Cognitive Performance Test (CPT). These are each on a 6-point scale with very detailed correlates for functional capacity and the need for additional resources. These objective scores are helpful in communicating with families, especially when financially

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difficult decisions are being made. Outside resources are frequently recommended to families. The Alzheimer’s Association has numerous online helps, caregiver support groups and 24/7 phone helpline (www.alz.org). A joint venture between many stakeholders in Minnesota is called ACT on Alzheimer’s (www. ACTonALZ.org). This organization is highly collaborative, engaging a broad network of organizations and communities. I am especially impressed with the desire to make communities “dementia friendly.” Professional resources are available as well. Another unique and helpful resource for families is the website and training for “Validation Therapy.” Naomi Feil, MSW, ACSW developed the technique of validation therapy “in response to her dissatisfaction with the traditional methods of working with the severely disoriented old-old people.” (www.vfvalidation.org, biography). The video of her singing to Gladys Wilson on the home page of this website should be mandatory viewing. The website has a wonderfully concise description of the theory behind her “methods,” and offers many training sessions. I frequently recommend this resource to families struggling with how to interact with their demented loved ones. There is nothing quite so helpful, however, as a clinician sitting at the bedside explaining the findings of dementia, its severity level, and treatment/care options. This is time consuming, but valuable in developing trust with the family. Front Line Staff

It is the front line staff in LTC who delivers the most care and interaction with dementia residents. Their training is utterly critical to promoting effective care for these residents. Dignity is the key ingredient to promoting effective dementia care. At Presbyterian Homes & Services, we provide training in two specific ways. The DOVE™ program (Dementia Orientation Values Education) emphasizes the strengths and skills of the dementia resident in three areas: Life Skills, Life Enrichment, and Self-Care. Another program is called Liberty Personally Designed Living,™ which emphasizes MetroDoctors

*Financing health care changes as patients progress from an acute illness to chronic care. Most acute care expenses are covered by Medicare Part A. For those qualifying for a rehabilitative stay (with a 3-day qualifying hospital stay) Medicare Part A covers most of the expense of transitional care in a skilled nursing facility. Medicare benefits continue until the patient reaches their therapy goals or “plateau” in their improvement. There is a 100-day limit to each episode of care, but the full 100 days are rarely used. The decision to end therapy is an attempt to conform to Medicare guidelines, but does shift the burden of payment to the patient or family. This decision point forces choices about discharge to less expensive living arrangements: the patient’s home, assisted living or a long term care facility. Home health care (nursing services or patient care assistants) may be used in assisted living and home environments to mitigate risk created by dementia and/or mobility limitations. These are usually paid privately by the family. These are difficult and expensive decisions. Very few assisted living apartments are paid for by medical assistance. The “elderly waver” portion of medical assistance will pay for a limited number of assisted living apartments. Patients remaining in long term care usually incur a “spend down” — utilizing their assets until they qualify for medical assistance. This often includes the sale of the family home, sometimes displacing adult children living in the home. resident-centered care. It asks the resident to describe “My Best Day,” and then incorporates those preferences into the care plan. Household “Chat Circles” encourage the resident community to mutually design their environment and activities. Other organizations have similar training programs. Resident-centered care promotes the dignity of the dementia resident. The Alzheimer’s Association has online training resources for family and staff caregivers in 4, 6 and 8 hour blocks with certification, if desired. Many facilities use these resources for new staff working on dementia care units. As medical providers, we must use our interactions with staff nurses and others as educational opportunities. For example, every time we are asked to prescribe a sedative or antipsychotic for “agitation” we must engage in an educational dialogue with the staff: What led to the agitation; have we considered a medical cause; can you use redirection/delay/validation to reduce the behavior; or can the family come to ease their distress? There is a thought process that needs to develop in our nurses (and ourselves) that views behavior like an abnormal vital sign, not simply a need for a medication. We have reduced the use of antipsychotics in many

The Journal of the Twin Cities Medical Society

nursing homes from 20-25% to fewer than 10%. This is due to a concerted effort to: 1) use the interdisciplinary team approach; 2) understand the ineffectiveness of most of these medications; and 3) believe that the individual interactions by the frontline staff are the most therapeutic treatment available. Summary

Caring for dementia patients in LTC means developing a team of well-trained caregivers who communicate clearly with referral sources, engage with families, and learn to promote dignity for older adults as a primary therapeutic effort. Clinicians have a strong supportive role in nurturing this process. Gandalf gives of his own life in the mines of Moria to promote the safety of the “Fellowship.” While we give of ourselves, we hope the patient and their family will succeed in this battle against fear and darkness. John Mielke, M.D., CMD is an Internist/ Geriatrician who specializes in care of the elderly in nursing and assisted living facilities. He is a Certified Medical Director and Past President of the Minnesota Medical Director’s Association. He is the Chief Medical Officer of Presbyterian Homes.

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Alzheimer’s Disease: The Future of Diagnosis, Prevention and Treatment Contributed by Michael Rosenbloom, M.D.

Introduction Alzheimer’s disease is the most common cause of dementia, accounting for 60 to 80 percent of cases and affecting 5.3 million individuals. It is also the sixth leading cause of death and the only one of the top 10 causes of death for which there is no treatment, prevention or cure.(1) An estimated 90,000 Minnesotans have the condition. Although the prevalence and associated costs of Alzheimer’s disease are expected to triple by 2050, 27-81% of physicians may fail to recognize the disease.(2) In addition, the last time the U.S. Food and Drug Administration (FDA) approved a drug for Alzheimer’s was more than 10 years ago. Fortunately, dementia research conducted in Minnesota and throughout the country is expected to make significant progress in diagnosis, prevention and treatment of Alzheimer’s. Diagnosis A definite Alzheimer’s diagnosis requires pathological confirmation of cerebral amyloid plaques and neurofibrillary tangles from brain tissue. Despite the reliance on diagnostic measures such as cognitive screening tests, neuropsychological testing, laboratory studies and neuroimaging, clinicians can, at most, provide a diagnosis of “probable Alzheimer’s.” Thus, Alzheimer’s is distinct from other chronic conditions such as diabetes or cancer in that the pre-mortem diagnosis is never guaranteed; standard diagnostic tests’ sensitivity and specificity for Alzheimer’s are 70.9 to 87.3% and 44.3 to 70%, respectively.(3) Following the release of the revised 2011 National Institute on 18

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Aging-Alzheimer’s Association criteria for Alzheimer’s,(4) this condition is now viewed as existing on a continuum of three separate stages: preclinical, mild cognitive impairment and dementia. Whereas mild cognitive impairment and dementia were already well-defined, the preclinical stage — a state in which patients lack cognitive symptoms but have evidence of Alzheimer’s-related brain changes — emerged as a research focus. In support of this concept, investigations of asymptomatic carriers of autosomal-dominant Alzheimer’s disease have shown disease-related changes such as altered cerebral amyloidosis and increased spinal fluid tau 15 to 25 years before the expected disease onset.(5) The concept of preclinical Alzheimer’s disease has inspired an explosion of research pertaining to serum, cerebrospinal fluid and imaging biomarkers intended to facilitate identification of Alzheimer’s disease. Alterations in cerebrospinal fluid levels of Abeta42 (decreased), tau (increased) and phosphotau (increased) have been documented in early-stage Alzheimer’s.(6) In addition, cerebrospinal fluid studies are occasionally used clinically to support a diagnosis. Amyloid positron emission tomography (PET), which consists of administration of a radioactive ligand that specifically binds to brain amyloid, has enabled clinicians and researchers to detect amyloid plaques in vivo. The earliest amyloid PET scans used Pittsburg Compound B, a carbon (C)11 radioisotope with a 20-minute half-life, which limited scanning to institutions with cyclotrons. However, fluorine(F)18 tracers, which have half-lives of 110 minutes, have enabled this diagnostic technique to be used

in clinics throughout the country. Although three F18 compounds are FDA-approved (flobetapir, flutametamol and florbetaben), the Centers for Medicare & Medicaid Services ruled in 2013 that the evidence was insufficient to conclude that amyloid PET imaging was necessary for diagnosis or treatment of Alzheimer’s. The Imaging Dementia Evidence for Amyloid Scanning trial (IDEAS), led by the Alzheimer’s Association and the American College of Radiology Imaging Network, is a study designed to assess the practical clinical application of amyloid PET imaging in atypical mild cognitive impairment and dementia. This investigation is measuring the impact of this imaging modality on medical decision-making and health care usage. A total of 18,488 Medicare beneficiaries aged 65 and older will be enrolled over 24 months at roughly 200 sites throughout the United States. If evidence suggests that this diagnostic procedure significantly affects clinical care, amyloid PET imaging could be reimbursable for atypical presentations of mild cognitive impairment and dementia. The HealthPartners Center for Memory and Aging in Saint Paul, MN is a physician referral and imaging site for the IDEAS study. Confirmation of cerebral amyloid is necessary but not sufficient for a diagnosis of definite Alzheimer’s disease. Whereas amyloid imaging was an important step

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The Journal of the Twin Cities Medical Society


in documenting the pathological signature of Alzheimer’s disease, this test is limited in that it fails to provide any information related to the deposition of neurofibrillary tangles and neurodegeneration — both common pathological changes in Alzheimer’s. Tau-PET imaging is the most recent imaging biomarker to detect brain pathological changes; the technique not only enables assessment of aggregated tau but also allows visualization of the neuroanatomical distribution. Specifically, Mayo Clinic in Rochester, MN has been using the PET tracer 18F-AV-1451 in both preclinical and Alzheimer’s disease, finding that imaging results effectively track disease progression. Between the IDEAS study and ongoing investigations into tau-PET imaging, the future of the diagnosis of Alzheimer’s may be simplified. However, whether PET imaging with radioactive ligands will revolutionize the diagnosis and treatment of Alzheimer’s disease remains to be seen. In addition to PET imaging, cognitive screening may be another way to facilitate early diagnosis of Alzheimer’s. Minnesotabased health care organizations, including Allina, Essentia, and HealthPartners, have explored or are exploring the role of cognitive screening in asymptomatic elderly subjects and its effects on health care outcomes. Prevention One of the most common questions is whether Alzheimer’s disease is preventable. Longitudinal cohort studies have shown that the risk of late-life dementia is decreased in individuals with routine physical activity, social activity and cognitive stimulation. In addition, effective measures to reduce physical inactivity, depression, smoking, midlife hypertension, midlife obesity and diabetes may reduce the incidence of Alzheimer’s by up to one third.(7) The design of clinical trials on the prevention of Alzheimer’s disease is particularly challenging due to the lack of a definitive predictive biomarker and the indolent disease progression. Consequently, a variety of multisite clinical trials are following and treating populations at highest risk for AD. The Alzheimer’s Prevention Initiative, a collaboration of the Banner Institute, the pharmaceutical industry and the National Institute of Health, is a longitudinal study of an extended family in Colombia carrying the presenilin 1 mutation in which MetroDoctors

offspring have a 50% chance of developing autosomal-dominant Alzheimer’s. In this condition, cognitive decline typically manifests by age 45. The Autosomal Dominant Alzheimer’s Disease Trial is testing the effects of the anti-amyloid antibody crenezumab in delaying cognitive symptoms in this population. Likewise, the Dominantly Inherited Alzheimer’s Network through Washington University is investigating longitudinal biomarkers in disease carriers. The Anti-Amyloid Treatment in Asymptomatic Alzheimer’s study, funded by the National Institute on Aging, Eli Lilly and Company and several philanthropic organizations, is aimed at preventing Alzheimer’s. The study will enroll 1,000 adults aged 65 to 85 with positive amyloid PET studies (i.e., biomarker evidence for Alzheimer’s) but no evidence of cognitive impairment. Eventually, subjects will receive an investigational amyloid antibody treatment. Outcomes related to cognition and development of Alzheimer’s will be compared between the investigational drug and placebo group. Mayo Clinic is a research site for this trial. Treatment The limited number of cognitive-enhancing and disease-modifying Alzheimer’s therapies has promoted extensive investigation into potential therapeutic agents. Since cerebral amyloidosis was identified as one of the earliest Alzheimer’s disease-related changes, numerous ongoing clinical trials have been conducted to inhibit the amyloid pathway in early-stage disease. Previously, clinical trials recruited patients with mild to moderate Alzheimer’s disease. However, the current trend is to identify subjects at the earliest stage detectable in the clinical setting, namely mild cognitive impairment or prodromal Alzheimer’s disease. Merck is studying the effects of a beta-secretase 1 inhibitor intended to block the production of amyloid on the progression of mild cognitive impairment to Alzheimer’s disease in prodromal Alzheimer’s. In addition, Genentech is conducting a phase 3 clinical trial of crenezumab, which binds specifically to Abeta peptides in subjects with mild cognitive impairment or Alzheimer’s. In addition to cerebral amyloidosis, the Alzheimer’s disease brain shows impairments in central nervous system insulin signaling and metabolism. Findings

The Journal of the Twin Cities Medical Society

indicating impaired insulin production and signaling have linked Alzheimer’s disease and diabetes mellitus. Consequently, Alzheimer’s disease has been called a “type 3 diabetes mellitus of the brain”.(8) These insulin deficits have provided the scientific foundation for two ongoing clinical trials in Alzheimer’s disease. The National Institute on Aging-funded Study of Nasal Insulin to Fight Forgetfulness is testing intranasal insulin in mild cognitive impairment and Alzheimer’s at sites throughout the country, including Mayo Clinic. The HealthPartners Center for Memory and Aging is conducting a phase II, double-blinded, placebo-controlled trial of the rapid-acting insulin IN glulisine to measure its effects on cognition and disease progression in mild cognitive impairment and Alzheimer’s. Finally, Fang Yu, Ph.D., at the University of Minnesota is evaluating the effect of routine aerobic exercise on cognition in Alzheimer’s disease through the FIT-AD trial. Outcomes related to exercise also will be compared with traditional pharmacotherapy in this patient population. Conclusion Due to challenges associated with diagnosis, prevention and treatment, Alzheimer’s disease remains one of the most formidable chronic conditions. Ongoing research into the relationships among early-stage Alzheimer’s disease, amyloidosis and tau deposition will be critical in shaping the diagnostic approach and clinical trials of the future. In addition, novel treatments aimed at addressing the underlying mechanism of disease, whether it is related to amyloid deposition, tau aggregation or central nervous system metabolic disarray, provide optimism for an eventual treatment or cure for this devastating neurodegenerative disease. Michael Rosenbloom, M.D. is a board certified Neurologist and Director of the HealthPartners Center for Memory and Aging. His clinical and research focus includes FDG-PET and PIB imaging in focal presentations of Alzheimer’s disease, rapidly progressive dementia, initial clinical symptoms in patients with frontotemporal dementia spectrum disorders, and therapeutic interventions for dementia. References available upon request.

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Dementia

Treating Alzheimer’s With a Big Dose of Policy

A

lzheimer’s disease (AD) is often front-page news: a celebrity reveals a new diagnosis, potentially promising results are featured from a clinical trial or a study in genetically engineered mice, or a new risk factor or theory is proposed. How much do we really understand about AD? Among the top 10 causes of death in America, AD is the only one that cannot be prevented, cured, or substantially slowed, and, of the five FDA-approved drugs available to treat the symptoms of AD, none materially alters its progression. More than 100 years after the first description of the neuropathology of AD, and after decades of important discoveries about genetic, lifestyle, and other risk factors and cellular and molecular mechanisms, we still lack a comprehensive theory to explain the cause(s) of AD and its close (but not universal) association with aging, and disease-modifying therapeutics. What does this mean for the approximately 5.4 million people living with AD in the U.S. today? There is much we can do now to improve the outlook for people with AD. One critical area of opportunity is within our healthcare delivery systems. Dementia has all too often been hidden — more than half of those affected have not been diagnosed, and among those who have, many patients and families have not been made aware of it by a clinician.1 Physicians have historically been skeptical about diagnosing a progressive condition, when medical treatments are of limited benefit and healthcare institutions have invested By Soo Borson, M.D., and Patricia Carlson, MPH

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Soo Borson, M.D.

Patricia Carlson, MPH

few resources in the specialized medical and psychosocial approaches that can help their patients.2 As the epidemic of agerelated neurodegenerative dementias has emerged in our increasingly long-lived population, its impact on health care delivery and systems — not just on patients and families — has sounded a call for systemic and policy reforms in the way we approach dementia in the clinic and in our communities. Several of Minnesota’s major healthcare systems are taking the lead in defining how to organize what’s needed for highquality dementia care. Developments in research have energized these efforts: practical case-finding tools have been validated and tested in general medical settings;3 diagnostic standards for AD and related dementias have been clarified;4 and a substantial evidence validates structured interventions to help family caregivers learn about and manage complications of AD and other dementias, particularly the disturbing changes in behavior that may occur as a consequence of changes in

brain function.5 At the same time, ACT on Alzheimer’s, created to guide implementation of Minnesota’s Alzheimer’s plan, synthesized an evidence-informed framework for moving from dementia case-finding to diagnosis and management and activating communities to become more aware of dementia. The framework also provides locally-driven education and tools to improve community-based services to individuals living with dementia and their caregiving families. ACT on Alzheimer’s toolkits are freely available online (www. ACTonALZ.org), and have been implemented in pilot studies at Essentia Health, HealthPartners, and Allina Health as well as several other healthcare systems in Minnesota and elsewhere, helping to shape policy as its efforts have ‘gone national’ as “Dementia Friendly America.” Warnings have been sounded for several decades about the consequences of population aging for brain health and healthcare delivery, but now are a central focus of new federal legislation and Medicare policy. The National Alzheimer’s Plan

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(“NAPA”), in a series of recommendations and milestones by its Advisory Council of researchers, clinicians, and services and policy experts, has articulated strategies for enhancing the productivity of research on basic mechanisms of neurodegenerative disease and development of new biological treatment targets and new therapeutic agents. These goals are now reflected in a large increase this year in federal research funding. In 2016, NAPA began to address the need for better data on the epidemiology of dementia, earlier detection, standardized approaches to diagnosis and management in health care settings, stronger support of caregiving families, and firmer linkages between health care and community-based organizations.6 Additionally, the Centers for Medicare and Medicaid Services (CMS) have come forward with new health care benefits that, if implemented widely, could transform health care. In 2011, CMS offered the Annual Wellness Visit (AWV), the first to explicitly call for identification of cognitive impairment as part of its broad-based patient health risk assessment. Widely misunderstood and disappointing in uptake nationwide (only about 11% of Medicare recipients take advantage of this free-to-consumer benefit),7 the AWV was not strongly promoted to healthcare providers or patients as a valuable new service for older adults that focuses on maintaining and improving health rather than treating disease. Nevertheless, some healthcare systems have embraced the AWV (the Twin Cities area is a ‘hot spot’ for implementation on the Dartmouth Atlas map)7 and worked to implement recommended strategies for detection of cognitive impairment.8 Other new CMS benefits followed the AWV, including Transition Care Management (aimed mainly at reducing hospital readmissions) and Chronic Care Management (focused on continuity of care and adherence support), both of which could substantially improve overall care of older people, especially those with multiple chronic conditions and those with dementia, whose rates of care transitions,9 potentially preventable MetroDoctors

admissions,10, 11 and readmissions,12 can be far higher than for cognitively normal older people. Now CMS is working to craft another new benefit specific to dementia and focused on comprehensive care planning for patients who have received a dementia diagnosis. The HOPE for Alzheimer’s Act — “Health Outcomes, Planning, and Education for Alzheimer’s Act” (S 857/ HR 1559), sponsored by the Alzheimer’s Association, calls for comprehensive assessment of the key domains adversely affected by dementia, including evaluation of patients’ cognition, mood and behavior, everyday function, safety, including medication management, and driving; review for high-risk medications; and assessment of caregivers’ needs. These elements are combined as the basis for constructing an individualized care plan. Elements of the care plan include advance care preferences and planning, appropriate management of neuropsychiatric and behavioral symptoms, and, as appropriate, referrals to community-based services for patients and caregivers. Development of the care plan is meant to be a joint effort between a clinician, other members of the clinical team, and the patient and family, to embody the principles of person-centered care13 as applied to the patient and his/her key care partners, and to be documented and shared widely with all who are involved in care. The HOPE for Alzheimer’s Act explicitly calls for provider education about the content and implementation of the new dementia care planning benefit, to obviate the gap in uptake that limits the reach of the AWV benefit. Minnesota has been a leader in health care reform, extending back to the 1960s, when legislation first established the Medicare program. New opportunities to improve the quality of health care provided to people living with dementia pose new challenges to clinicians and healthcare systems: to embrace dementia as a complex but manageable chronic condition with many secondary effects on the health of patients and families; to structure healthcare organizations for better chronic care management functionality; to define teamwork

The Journal of the Twin Cities Medical Society

components essential in dementia care; and to support clinicians at the point of care, by dementia-focused electronic health record designs that provide essential information, referral recommendations, and population-based tracking. Minnesota Brain Aging Research Collaborative (M-BARC), a project of the University of Minnesota N. Bud Grossman Center for Memory Research and Care in partnership with local healthcare providers and systems, seeks to advance these goals. For more information about M-BARC, visit m-barc.net. Soo Borson, M.D., Professor Emerita, University of Washington; Adjunct Professor, University of Minnesota, and Patricia Carlson, MPH, Associate Program Director, N. Bud Grossman Center for Memory Research and Care, University of Minnesota. Co-Leads, Minnesota Brain Aging Research Collaborative (M-BARC), m-barc.net. References available upon request.

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Dementia

Traumatic Brain Injury as a Risk Factor for Dementia: Where is the Science and What are its Implications? The relationship between traumatic brain injuries (TBI), chronic traumatic encephalopathy (CTE) and dementia is complex. Much media attention has been focused on CTE, and its occurrence as a consequence of sports participation. However, we would argue that the consequences of brain injury are far more vast and pathophysiologically complex than CTE. We briefly summarize below the current scientific literature with regards to CTE and dementia associated with traumatic brain injury. Chronic Traumatic Encephalopathy

CTE’s history began in New Jersey with forensic pathologist Harrison Stanford Martland first describing a distinct neurologic entity in the brains of deceased boxers in 1928 with the term “dementia pugilistica”. By 1957, there were a handful of case reports published and the eminent Queens Square neurologist MacDonald Critchley coined the term “Chronic Traumatic Encephalopathy” based on his findings of Parkinsonian symptoms in 69 living boxers.1 In 1969 Anthony Herber Roberts, also from Queens Square, published an epidemiologic study of 250 living boxers and found CTE, then characterized as a clinical disorder of motor symptoms and dementia, in 17% of them. In 2005, when neuropathologist Bennett Omalu reported finding CTE in the American football player Mike Webster,2 the British were simply not amused. Calls to retract the paper arose from concern that the American CTE bore no microscopic By Jessica Flores, MS2 and Uzma Samadani, M.D., Ph.D. MetroDoctors

Jessica Flores, MS2

resemblance to its original counterpart described rigorously in multiple cases at Queens Square by neuropathologist Dr. J.A.N. Corsellis. The British argued that Omalu was observing a distinct problem both in clinical symptoms and under the microscope. The neuropsychologist Jim Andrikopoulos wrote an editorial to the British Medical Journal saying “CTE, as defined in America, is not a neurological entity, but is a culture-specific social phenomenon.” But CTE in America was not just one entity. Independent from Omalu, researchers at Boston University (BU) led by neuropathologist Ann McKee both published and went to the media with their findings, ultimately telling PBS’ Frontline that CTE was present in 87 of 91 former professional football players. Unlike Omalu, who stated that a single concussion can lead to CTE, the Boston group indicated that more than one brain injury has to occur. The pathologic findings were different in Omalu-CTE and Boston-CTE,

The Journal of the Twin Cities Medical Society

Uzma Samadani, M.D., Ph.D.

and neither resembled British-CTE which could be diagnosed in the living. Multiple scientific reviews of both forms of the American CTE argued that it could only be diagnosed in the dead. With confusion rampant in the pathology literature, the government stepped in, sponsoring “The First NINDS/ NIBIB Consensus Meeting to Define Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy” which occurred on February 25-26, 2015. Twenty-five cases were reviewed by seven pathologists in advance, and a definition of CTE with four subtypes was established. 3 In the meantime, Kevin Bienieck and colleagues at Mayo Clinic reported in December 2015 that one third of all males participating in contact sports were at risk for CTE. 4 Sixty-six males who participated in contact sports were chosen as subjects, while 198 males who (Continued on page 24)

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Dementia Traumatic Brain Injury (Continued from page 23)

had no past involvement in contact sports were the controls. Only three of the former athletes had been diagnosed with concussions in their lifetime, yet the researchers found evidence for CTE in 21 out of the 66. However, of the 198 subjects in the control group, 33 had documented cases of head trauma, but none showed evidence of CTE. The paper states, “Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features.” Basically, both subjects with brain tangles indicating CTE and subjects who lacked tangles exhibited no symptoms while alive. This work suggested that contact sports were associated with CTE, but that CTE had no clear association with head trauma nor was it associated with any symptoms, including dementia. In that same journal, Acta Neuropathologica, where the Mayo Clinic study appeared, a paper was published by Helen Ling and colleagues.5 The study compared brains of people who died with neurodegenerative diseases to control subjects. The paper found that “the prevalence of CTE in [people with] neurodegenerative diseases (11.8%) was statistically the same as in controls (12.8%).” They also found that patients with CTE died at a mean age of 81 years and that “most positive cases [were] likely to be clinically asymptomatic.” The phosphorylated mislocalized tau protein, pathognomic for CTE, was not pathognomic for dementia or any other clinical neurodegenerative disease. CTE was found under the microscope in equal proportions in healthy, asymptomatic subjects and in subjects with dementia and other diseases. These studies raise questions regarding the clinical significance of the pathologic findings associated with CTE, which has been seen in both opiate abuse and with normal aging. Is it clinically relevant if athletes are at increased risk for CTE, if the disease has no symptoms? Far more importantly, even if there is not a clear association between CTE and dementia, 24

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one still has to consider the cognitive and psychologic consequences of brain injury, which are pathophysiologically diverse and as complex as they are consequential. Traumatic Encephalopathy Syndrome

Attempting to bridge the gap between pathological findings and symptom presentation, Dr. Nicole Reams and colleagues published a review in JAMA Neurology in June 2016. The paper explained that CTE was not a clinical problem but that an independent unrelated disorder exists in living people called Traumatic Encephalopathy Syndrome (TES), which is the clinical manifestation of a progressive neurodegenerative disease that may result from head injuries.6 The authors proposed a classification scheme in which TES was ultimately a clinical diagnosis of exclusion, representing mixed pathophysiology. The relationship between CTE and TES was considered by Breton Asken and colleagues in Neuropsychology Review in August 2016, who noted that there are many factors to consider when diagnosing CTE because many symptoms of TES, including dementia, can be non-specific for CTE.7 Moreover, the authors question the variability of symptoms of TES that present in some, but not all, people who suffer from repetitive TBI. They argue that biopsychosocial factors such as sport-specific demographic biases, like a lower socioeconomic background, are correlated with more aggressive behavior and higher rates of depression in adolescents, which may influence cognitive development throughout a lifespan. We would posit that the pathophysiology of TES encompasses at a minimum: cortical spreading depression/spreading depolarization, chronic sequela of diffuse axonal injury, endocrine dysfunction, iron toxicity from microhemorrhage, hypoxic/anoxic injury, and astroglial scarring (blast). Isolated Brain Injury Associates With Motor Neuron Disease but Not Dementia

A multi-institutional study with 45,190

person-years of follow-up investigated the association between brain injury and dementia. In the largest prospective study published to date on this subject, Dr. Paul Crane and colleagues published in JAMA Neurology in July 2016 describing their results in TBI with loss of consciousness (LOC) and the risks of late-life onset neurodegenerative and pathological disorders.8 Out of the 7,130 subjects that were free of dementia at enrollment, 1,589 underwent autopsies and 2,879 had a past history of TBI with LOC. They did not find a relationship between TBI with LOC and latelife dementia, Alzheimer’s disease, neuritic plaques, nor neurofibrillary tangles. Moreover, they admitted having “ample power to find such a relationship, but there was not one to find.” However, they did find a significant correlation for TBI with LOC and Lewy body accumulation, Parkinson’s disease and progression of Parkinsonism. As the paper above suggests, most individuals with isolated head injuries do not have an elevated risk for developing CTE nor dementia, but are at risk for motor system disorders like Parkinson’s disease, like the late boxing champion Mohammed Ali suffered. Brain Injury has Psychiatric and Other Consequences

The largest epidemiologic study published to date in PLOS on August 23, 2016, followed 104,290 people under age 25 with brain injury, comparing them to their unaffected siblings for a median of eight years. Those who experienced a mild or moderate-to-severe TBI demonstrated an increased risk of 18-52% and 49%-200% respectively, for psychiatric inpatient hospitalization, disability pension and premature mortality. While this Swedish study did not detail the etiology of the injuries, it found that both severity and number of brain injuries worsened outcome.9 The study demonstrated that 9% of Swedes sustained a brain injury prior to age 25, and thus may be biased to include only more severe cases in which patients saw a physician and were rendered a diagnosis. Estimates in the U.S. and Canada have suggested that one quarter to one third of youth have sustained a concussion, with

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the majority not seeing a physician since symptoms are self-limited. Summary

Thus, it is clear that brain injury is absolutely, unquestionably injurious to the brain with complex multifactorial consequence. A single brain injury is unlikely to cause dementia but is associated with psychiatric consequence. Although the potential connection between CTE and NFL players has recently been popularized by media outlets such as 60 minutes and the movie Concussion, multiple brain injuries have impact far more complex than the diagnosis of CTE can explain. It is unclear whether reported anecdotal cases of CTE associated with clinical dementia, such as seen with studies published by the Boston University group and those seen in the movie Concussion, are results of ascertainment bias, repetitive TBI or multifactorial in origin. More robust studies with unbiased selection of subjects that prospectively look at brain injury in both athletes and nonathletes are necessary to objectively detect, classify and treat harmful effects of TBI. Sports participation/avoidance of sedentary lifestyle, which are known to decrease risk of hypertension, diabetes, dementia, cardiovascular disease and cancer, should be encouraged even as efforts to make sports as safe as possible are pursued. Neurosurgeon Uzma Samadani, M.D., Ph.D., is the Rockswold Kaplan Endowed Chair for Traumatic Brain Injury Research at Hennepin County Medical Center (HCMC), and an Associate Professor of Neurosurgery at the University of Minnesota. She can be reached at: Uzma.samadani@ hcmed.org. Jessica Flores is a second year medical student and American Heart Association Summer Research Scholar at the University of Minnesota. She is currently performing brain injury research in the laboratory of neurosurgeon Uzma Samadani M.D. Ph.D.

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Dementia

ACT Summit 2016 Building Plans to Act on Alzheimer’s

H

ealth care organizations are planning how to advance care and support for people with dementia and their caregivers. More than 135 health care leaders from across Minnesota at the ACT on Alzheimer’s Health Care Leadership Summit on September 29 participated in a working session to explore creative solutions for improving dementia detection and care in our organizations and influencing the national discussion around this disease. People with dementia and their caregivers at the summit asked that Alzheimer’s have similar care standards for diagnosis and follow-up as other chronic diseases and conditions, like heart disease, cancer and pregnancy. Research shows that delayed diagnosis and failing to connect people to supports often results in preventable crises. The summit’s call to action was clear: We need early detection and a team approach using care coordination to avoid more preventable crises and improve quality of life and care for people living with dementia. “Early detection and diagnosis are important in making the cognitive and emotional transition from wide-ranging, independent self-directed activities to collaborative shared activities,” said Marv Lofquist, Ph.D., a person with dementia, diagnosed early and living well to his full capacity, for over four years with the support of his wife. Dementia is personal. We’ve all been affected professionally or personally by dementia—every 66 seconds someone develops Alzheimer’s. The risk is highest for older African Americans, Latinos and women. “We know how to do this, and we 26

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have the tools,” said Penny Wheeler, CEO of Allina Health. “We just need to ACT. The time is now.” We all need to be part of the solution to reframe the challenge of dementia and focus on value-based care. We want to improve personal outcomes and experience, and reduce unnecessary utilization. Summit attendees committed to implementing

Shari Ling, M.D., Deputy Chief Medical Officer, Centers for Medicare & Medicaid Services (CMS) Medical Officer, Center for Clinical Standards and Quality, outlined the national perspective at the summit, conveying the role dementia plays in value-based care. She reviewed the current billing codes applicable to Alzheimer’s detection, diagnosis and

We need early detection and a team approach using care coordination to avoid more preventable crises and improve quality of life and care for people living with dementia. new action steps after the event, including: • Establish standardized protocols for identification, diagnosis and care coordination. • Implement use of the MiniCog screen for cognitive impairment in Medicare annual wellness visits during clinic rooming process and in all hospice and home health admissions. • Embed dementia algorithm in electronic health record. • Develop a clinical pathway similar to other chronic diseases for home health patients. • Form a care team and navigator to support people with dementia. • Pilot a dementia chronic care management program. • Incorporate dementia awareness into grand rounds. • Identify a physician champion. • Explore how dementia is incorporated into risk models.

post-diagnostic care, as well as potential reimbursement opportunities through the proposed changes to the 2017 Medicare Physician Fee Schedule. Minnesota can do better with our care delivery and supports. Ask how you can get involved in changing the future of dementia by contacting Michelle Barclay, ACT on Alzheimer’s, at mpbarclay@barclaygp.com or (612) 408-2910. ACT on Alzheimer’s is a statewide, multi dimensional collaboration seeking large-scale social change and building community capacity to transform Minnesota’s response to Alzheimer’s disease. A signature goal is to help health care providers and systems become dementia capable. Tools and resources for health care providers and systems are available at www.ACTonALZ.org/ provider-resources.

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TCMS Explores Climate Change and Role for Physicians

T

he TCMS Environmental Health Task Force recently surveyed Society members on your attitudes and knowledge regarding health effects of climate change. Although the response rate was low, useful information emerged. Three-fourths of respondents affirmed that in Minnesota, climate change, by extending our warmer wetter seasons and moderating our winters, has affected our health in many ways: • The prolonged pollen season has increased the incidence and prevalence of allergic disorders and asthma (also impacted by fossil fuel generated air pollution); • Increased vector winter survival and expanded vector geographic ranges leading to increases in incidence of vector-borne diseases; and • Documented higher rates of heart and lung disease; and more flood-related outbreaks of water-borne illnesses. It was interesting to compare this to similar studies from The American Thoracic Society and the American Academy of Allergy Asthma and Immunology. Eightyfive percent of their respondents agreed that climate change has and will have an effect on their patients. Most major health organizations have issued policy statements expressing concern over the health implications of climate change. These include the World Health Organization, the American Public Health Association, the Centers for Disease Control, the AMA, the MMA, the American College of Physicians, the American Academy of Family Physicians, the American Academy of Pediatrics, the American Thoracic Society, Harvard School of Public Health, KaiserPermanente, and Cleveland Clinic. Nursing organizations are similarly concerned. The Environmental Health Task Force is continuing to explore opportunities for physicians to respond, on a local level, MetroDoctors

to climate change and its effects on our patients. In the meantime, we encourage you to look into this issue. Here are some useful resources: 1. Making the Connection: Climate Changes Health — APHA and ecoAmerica cosponsor a four-part webinar series investigating the health impacts of climate change. The series explores the connection between climate change and key areas of our health. http:// www.apha.org/climate-changeshealth?utm_medium=email&utm_ source=webinarpolicyemail&utm_ca mpaign=ecoamericawebinar1replay& utm_content=climatechangeshealth.

The Journal of the Twin Cities Medical Society

YOU

2. Climate Change in Minnesota: Minnesota Climate and Health Profile Report. http://www.health.state.mn.us/ divs/climatechange/climate101.html. Environmental Health Task Force Members: Ryan Greiner, M.D., Chair Jennifer Kuyava, M.D, Vice-Chair Kristen Bastug Eric Beck, M.D. Mark Menzel, M.D. Mark Nissen, M.D. Stefan Pomrenke, M.D. Bruce Snyder, M.D. Jordan Weil

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For Physicians in Minnesota. . .

Hearing Loss, Dementia And Your Patients Hearing loss is a leading cause of dementia. A medical study at Johns Hopkins Medical Center found that hearing loss can increase your patient’s risk of developing Dementia by 200-500%. Social isolation, cerebral atrophy (aka. brain shrinkage) and increased cognitive load (e.g. the amount of work your brain uses to hear) are considered to be the basis of hearing lossinduced dementia - even for individuals with a mild hearing loss.

Refer Patients for a Simple Hearing Evaluation

Hearing Loss & Dementia How are they Connected?

But.... recent evidence from Columbia University finds that restoring hearing with today’s leading treatment options could prevent or slow down the development of Dementia.

1. Social Isolation 2. Cerebral Atrophy 3. Cognitive Overload (i.e. Working Too Hard To Hear)

Are Your Patients At Risk? Establish Your Risk.

Individuals with hearing loss are at a increased risk for developing cognitive decline and Dementia. While the risk increases with degree of hearing loss, it is important to note that even a mild hearing loss (e.g. having some difficulty hearing in background noise, turning up the TV a bit more than your spouse / family, having a hard time following a conversation in the car, etc.,) can increase your patient’s risk of Dementia.

www.AudiologyConcepts.com

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The Convenings Meaningful Conversations About Living and Dying Well

T

he Convenings is a unique, multi-layered community engagement program designed to inspire and motivate individuals and families across Minnesota to have meaningful conversations about living and dying well. This exciting new effort builds on the work of two significant initiatives: Honoring Choices Minnesota, a state-wide effort to engage Minnesota families in end-of-life care decisions, and an award winning series of broadcast conversations and book by journalist Cathy Wurzer that chronicles the life of Bruce Kramer, former Dean, University of St. Thomas College of Education, who lived an extraordinary life in the face of terminal illness. The goals of The Convenings are to: • Inspire people to think about and discuss their choices for living and dying well. • Evoke a sense of urgency for such conversations. • Build/spark communities of care throughout the state. • Empower community leaders with skills and resources to stimulate conversation and increase public awareness of living and dying well. • Share stories about and ideas from what other communities are doing. These goals reflect a growing need for authentic discussion and thoughtful decision making as society grapples with an ailing and rapidly aging population.

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Senior Physicians Association Fall Meeting Vice President for Health Sciences and Dean, University of Minnesota Medical School Brooks Jackson, M.D. was the guest speaker at the September 27, 2016 meeting of the Senior Physicians Association. Presenting an “Update on the Medical School,” he stated that the medical school and Twin Cities Medical Society have shared interests in advancing health care and are partners in training of students — our future leaders. Priorities included: cultural diversity; the cost of medical education/debt; research; and a legislative agenda. The first meeting of the Senior Physicians Association for 2017 will be held on February 28. “Understanding Aid in Dying” will be presented by Rebecca Thomas, M.D. — A topic that is sure to generate much discussion at the upcoming legislative session. Please calendar these future meeting dates and watch your email for additional information: February 28, 2017 May 2, 2017 October 10, 2017 Questions? Contact Nancy Bauer at TCMS (612) 623-2893; nbauer@ metrodoctors.com.

CAREER OPPORTUNITIES

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November/December 2016

Marilyn Joseph, M.D., President, Senior Physicians Association, and Brooks Jackson, M.D., Vice President for Health Sciences and Dean, University of Minnesota Medical School.

See Additional Career Opportunities on page 31.

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The Journal of the Twin Cities Medical Society


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November/December 2016

31


LUMINARY of Twin Cities Medicine By Marvin S. Segal, M.D.

SANNE DAIL JONES MAGNAN, M.D.

Our Luminary has had a long, pleasant and successful career. That pathway has experienced a variety of fruitful and circuitous twists and turns, and one can’t help but wonder if a common thread has been an operative element throughout that journey. Let’s just see if we can solve the mystery of a common linking variable as we explore that career. Born and raised in North Carolina, Dr. Sanne Magnan followed her pharmacist father into the same profession — earning her bachelor’s degree in that state’s University. During her educational pursuit, she had serious thoughts of attending medical school one day. Soon after, this young female pharmacist moved to Minnesota and found our state’s nurturing environment and the unwavering support of her husband essential in leading her first to a Ph.D. in medicinal chemistry and then an M.D. in 1983 at our U of M. There followed an internal medicine residency at that alma mater and a variety of clinical practice and teaching positions in adult health care at Ramsey/ Regions/HealthPartners over portions of the ensuing decade. Sanne’s initial administrative duties as an Associate Medical Director with Blue Cross began in the early 1990s. There followed, over the next few years, positions of increasing accountabilities with that organization in the disciplines of preventive care, tobacco reduction and health improvement. She then ascended to the Vice Presidency and Medical Directorship for Consumer Health at Blue Cross with the significant responsibilities of case management, disease management and consumer engagement — all carried out while continuing her clinical work as a part-time staff physician in Ramsey’s tuberculosis clinic and Adjunct Faculty activities with the U of M Medical School. Two periods of activity as the President/CEO for the prestigious Institute for Clinical Systems Improvement (ICSI) totaling 6+ years were interrupted by over three years of service as the Commissioner of Health for the State of Minnesota. Playing prominent roles in the assortment of Dr. Magnan’s profound professional pursuits were, as she modestly describes them, “wonderful opportunities coupled with dedicated mentors.” She actively searched for chances to broaden the horizons of her organizations and her communities, identified them and — being at the right places at the right times — stepped 32

November/December 2016

through those “series of doors.” Those meaningful steps resulted in a broad array of benefits to our medical profession and the welfare of the patients to whom we minister. Along the way, Sanne’s leadership skills were sharpened. She applied her medical and scientific background with newfound capabilities in finance, audit and currently mushrooming technological initiatives. All of those background competencies allowed her to marshal the forces necessary to lead in effecting successful care guideline acceptance and institution, and delve into the advancement of three important aims: improving the quality of patient care experiences, bettering the health of populations, and decreasing the per capita cost of health care. Dr. Magnan is now encouraged by the ongoing shift from volume to value-based care and payment — for which she has been a driving force — as she assumes new positions as both a Senior Fellow of HealthPartners Institute for Education and Research and Co-Chair of the Population Health Improvement Roundtable of the National Academy of Medicine. The good Dr. Magnan, who — in addition to her professional activities is an avid walker; an accomplished hosta gardener; a loving daughter, mother and wife; and the possessor of superb rhubarb recipes — loves tackling goals that bring people together to solve issues, actions that she has followed diligently where all stakeholders play a role and work together. So, we now have an answer to the mystery of that common thread weaving its way through the marvelous career of our LuminaryCOLLABORATION . . . just one of Dr. Sanne’s secrets of success. This last page series is intended to honor esteemed colleagues who have contributed significantly to Twin Cities medicine. Please forward names of physicians you would like considered for this recognition to Nancy Bauer, managing editor, nbauer@metrodoctors.com.

MetroDoctors

The Journal of the Twin Cities Medical Society


This Thanksgiving, carve out time for the conversation.

Profile for Twin Cities Medical Society

November/December 2016 - Dementia  

In this issue: The Research, The Epidemiology, Alzheimer's, Resource and Support Systems, Luminary of Twin Cities Medicine

November/December 2016 - Dementia  

In this issue: The Research, The Epidemiology, Alzheimer's, Resource and Support Systems, Luminary of Twin Cities Medicine

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