Battling Alzheimer’s Disease: Then and Now

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, 2016). These results (defended by several studies with regard to the significance of dendritic spines in memory processing) collectively support the claim that LTP-inducing optogenetics may serve as an effective component of future AD therapy. To boot, AD deficits (e.g. in solving everyday problems or making choices on a daily basis) may also be ameliorated through deep-brain stimulation (DBS) targeted at the ventral capsule/ventral striatum area (Scharre, 2016).

While all three instances of research offer hard scientific evidence regarding improvement of symptoms unique to AD, Fu’s research is particularly consistent with other neurological studies that specifically look into how inflammation increases as humans age and how it is inherently linked to many diseases common for the elderly (in this case, over 65), such as atherosclerosis, osteoarthritis, and consequently, Alzheimer’s. While inflammation is naturally a complex biological response for protection against harmful stimuli such as a pathogenic attack, its occasional abnormalities are in fact known to underlie a wide range of systemic conditions.

Although it is not included as a major example of research in this paper, the intriguing work of Professor Clive Holmes, along with that of his colleagues at the University of Southampton (UK) and King’s College London, includes the isolation of a cytokine vital to the acute-phase reaction of macrophages, TNF±. It has been found through this study itself that AD can, in a way, be diagnosed by monitoring levels of this protein in the bloodstream. Additionally, the study refers to possible treatment of the neuroinflammation associated with AD via a compound known as etanercept, a TNF± inhibitor used to mend autoimmune disorders that is in phase II clinical trials as of 2015 so that its potency against AD may be measured; it is however hypothesized to work by blocking CSF1R, a receptor needed for microglial activation (Fillit).

Multiple laboratory experiments have also uncovered the apparent effects of nonsteroidal anti-inflammatory drugs, such as 2-(4-isobutylphenyl) propionic acid or acetylsalicylic acid, on the advancement of numerous aspects of AD pathology, most notably the continual presence of dystrophic extensions and amyloid deposition, suggesting an increase in the housekeeping activities of microglia, including phagocytosis of cellular debris (Vlad, 2008). Yet another line of strong affirmation for the inflammation-Alzheimer’s link comes from large-scale analyses of thousands of participants for the detection of small variations in unusual and typical genotypes for AD. Alzheimer’s risk has, on the basis of the results of these studies, been tied to several genes involved in innate immunity, a primary group of nonspecific bodily defenses. One gene, TREM2, encodes for a novel monocytic/neutrophilic receptor and is of special interest to scientists. It has been found that homozygous or missense mutations within this locus may result in elevated likelihood for amyotrophic lateral sclerosis and Parkinson’s disease, as well as early onset forms of autosomal recessive dementia (due to impeded proteolytic maturation of microglia). Much of this research portrays AD as a logical progression of neurodegeneration in which accumulated oligomers (created as enzymes called secretases cleave precursor proteins) stimulate microglia to release an intricate series of extracellular signaling molecules, resulting in chronic inflammation. A significant portion of neuronal apoptosis as it occurs in AD may also be due to degranulation of microglia and rising amounts of reactive oxygen species, processes which can culminate in neurotoxicity. The previously mentioned interleukins mentioned in Fu’s research contribute heavily to deposition by acting as original mediators for phosphorylation (e.g. tyrosine kinase) cascades in microglia, gradually setting the stage for a hyperactive immune responseand thuscognitive dysfunction.

As of the present day, Alzheimer’s disease (AD) remains an indisputably debilitating and degrading illness that never fails to rob those in its grip not only of their societal and financial grounding, but also their individuality. As the Irish poet and playwright Oscar Wilde once rightly said, Memoryis the diary we all carry about with us. If not fixed, AD could cost Americans alone an estimated $1.1 trillion by 2050 in the totality of all its complications (Johns 2). In the fullness of time, AD lastly calls into question ethical predicaments that form the first barriers to a universal cure. After all, in our efforts to protract morbidity, we must not forget to treat humanely and with the best expression of care, love, and attention (Post 1932).

In order to gain a complete understanding of the pathophysiology of Alzheimer’s disease (AD) for avenues of treatment, it is necessary to conduct a study that examines the biochemical perspective of neural proteopathy, a term that denotes protein misfolding in cells of the human nervous system. For this purpose, it is important to examine the state of activation of microglia in different stages of AD for appropriate determination of the exact effect(s) of potential anti-inflammatory therapies. Therefore, evidence supporting the beneficial or detrimental performance of microglia in AD must be collected, primarily to aid in finding biomarkers for diagnostic or therapeutic interventions. With sufficient knowledge and practice, a panacea for the far-reaching dilemma of AD can surely be found.

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