Alzheimer’s Disease Research example

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Alzheimer’s Disease Research

The rapidly changing demographic situation accompanied by the aging of the population has triggered late-life dementia that is some of the most urgent problems of the modern psychiatry. The situation is associated with
steadily increasing frequency of dementias and particular severity of medical and social consequences. Alzheimer’s disease is one of the most common causes of dementia in the elderly and old age. It occupies a
relatively small place in the structure of psychiatric morbidity among elderly patients. However, the patients inevitably find themselves in a psychiatric hospital or a specialized mental health care facility due to the severe decay of mental activity and disability. Thus, Alzheimer’s disease is a serious social and health problem. The analysis of all factors that lead to its development, as well as early detection of symptoms and the development of new possible treatments are the main health challenges in addressing the issue.

Causes of the Disease
In fact, there are three main competing hypotheses that suggest an explanation of the possible causes of Alzheimer’s disease. According to the cholinergic hypothesis, the reason is in the reduced synthesis of the
neurotransmitter acetylcholine (Craig, Hong, & McDonald, 2011). The majority of existing therapies derive from this hypothesis since it is the oldest one (Craig et al., 2011). However, it enjoys little support in modern times because the efforts of medical professionals to correct the deficiency of acetylcholine have low efficiency.

The second one is the amyloid hypothesis. It suggests that the underlying cause of the disease is the deposition of the amyloid-beta peptide (Harrison & Owen, 2016). The gene that encodes a protein, which forms the amyloid-beta, is located on chromosome 21 (Harrison & Owen, 2016). A fact in support of the amyloid hypothesis is that the APOE4 gene, which is the primary genetic risk factor for the Alzheimer’s disease, leads
to excessive accumulation of amyloid in the brain tissues before the onset of symptoms (Selkoe & Hardy, 2016). Moreover, the transgenic mice’s brains deposit the fibrillar amyloid plaques (Selkoe & Hardy, 2016). It is an
important fact because their organisms produce a mutant form of the human APP gene. It is worth mentioning that other pathological symptoms that are characteristic of Alzheimer’s disease are also peculiar to transgenic mice (Selkoe & Hardy, 2016). Although an experimental vaccine has demonstrated the ability to clear the brain of amyloid plaques in early human trials, it had no significant effect on dementia.

Finally, there is one more major hypothesis. The correlations of accumulation of plaques with the loss of neurons have not been found. This fact supports the tau hypothesis, which states that the abnormalities …

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