Chelsie Norton
possible effects before choosing a side of the impending controversy. Cognitive enhancement is “the amplification or extension of core capacities of the mind through improvement or augmentation of internal or external information processing systems” (Bostrom, 2009, p. 311). A cognitively enhanced person profits from a procedure that improves function, not a procedure that fixes an existing problem. Therefore, any changes made to an embryo that tests positive for Down syndrome does not result in a cognitive enhancement. Cognitive function can be divided into three categories that all relate to how the senses capture and organize data: focusing on, understanding, and retaining information; and using it to control behavior through “reasoning and coordination of motor outputs” (Bostrom, 2009, p. 311). Thus, memory is a component of cognition and may be targeted through genetic enhancement to improve cognition. Genetic enhancement is a relatively new branch of biology with no regulations, laws, or widespread public opinions. To the novice researcher’s best knowledge no human trials have taken place nor have any significant conferences introduced the subject to the public. An ordinary citizen may not suspect enhancement is possible until he sees a “Be Smarter Now!” infomercial on television. Is it society’s duty to ask questions, or is it scientists’ responsibility to survey the public before taking action? This power struggle between the experts and the recipients may result in an outcry for regulation and honesty. Although controversial, genetic cognitive enhancement in humans and other mammals is feasible. The positive effects of transgenic experiments are seen in Doogie, transgenic mice engineered by Joe Tsien and his team in 1999 (Tang, 1999, p. 64). Tsien recognized Hebb’s rule, which states: Learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active. This implies that enhanced synaptic coincidence detection would lead to better learning and memory. If the NMDA (N-methyl-D-aspartate) receptor, a synaptic coincidence detector, acts as a graded switch for memory formation, enhanced signal detection by NMDA receptors should enhance learning and memory (1999, p. 63). Tsien over-expressed one of the NMDA receptors, NR2B, in Doogie to prolong the detection of synaptic coincidence. The results followed Hebb’s rule; Doogie displayed an increase in cognitive function and a sharper memory. The mice displayed no adverse side effects, seemed to mate and grow normally, and were indistinguishable from wild mice in behavior. Additionally, as the mice aged, they did not exhibit a severe decrease in memory function (Tang, 1999, p. 64). Tsien used an object recognition
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