Alzheimer’s disease (AD) is a chronic illness of extreme neural atrophy characterized by extensive memory loss, disorientation, and labored social communication/behavior. Often beginning after 65 years of age, AD constitutes between 60“70% of all dementia cases
(Duthey 6) and, by extension, afflicts between 35“50 million globally at any given time (Park). The tracking of AD is largely an arduous task, even with sophisticated neuroimaging such as tensor-based morphometry and cortical thickness mapping; however, due to its devastating toll, a treatment for it is still of great importance to medical professionals and sufferers alike. Fortunately, our 21st-century knowledge of AD and of its impact on one’s brain seems to furnish neuroscientists worldwide with more-than-adequate insight on how to develop novel treatments of unprecedented effectiveness for the disease. To the German physician Alois Alzheimer (who first stumbled upon AD back in 1906 by probing the case of Auguste Deter, then a 51-year-old woman admitted to the Frankfurt Hospital where he practised), today’s advances would indeed come across as astonishing considering all the progress made in the field over just 111 years.
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On the one hand, a hypothetical method involving precise control of the innate immune response in humans by virtue of IL-33 signaling is proposed in hopes of rescuing memory deficits (Fu, 2016). On the other hand, another method of therapy is proposed contradictory to the notion that AD halts the assimilation of new memories (Roy, 2016) by using optogenetic techniques. Lastly, the research of Roy is backed by evidence apropos of the therapeutic use of deep brain stimulation for treatment of neuromotor impairment (Scharre, 2016). While this paper does chiefly shed light upon the technicalities of these pioneers’ work and that of a few others, it remains worthwhile to note (as I will through the means of the paper) also the moral and socioeconomic implications of the research described herein.
In a groundbreaking investigation published in the Proceedings of the National Academy of Sciences (USA), the hidden role of interleukin-33 in fixing cognitive decline associated with Alzheimer’s comes to light with the discovery that its injection in APP/PS1 transgenic mice undoes deficiencies in contextual memory and synaptic plasticity unique to AD’s pathology
(Fu, 2016). Upon further research, it was revealed that IL-33 not only reduces the accumulation of soluble peptides (by promoting the phagocytic activity of microglia) but also discourages the adverse inflammation that’s so closely linked with the disease in discussion.
On the other hand, another such investigation published in the Nature International Journal of Science proves the amnesia characteristic of early AD to be an outcome of compromised memory retrieval rather than compromised memory storage. An AD model involving transgenic mice of various ages was extensively studied via the light-specific stimulation of hippocampal engram cells so to rescue lost episodic memories by way of optogenetic technologies (Roy,
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