A Comprehensive Review on Alzheimer’s Disease its Pathogenesis, Epidermiology, Diagnostics and Treatment
DOI:
https://doi.org/10.55544/jrasb.2.4.8Keywords:
Alzheimer disease, Diagnosis, Pathogenesis, Therapeutic effectAbstract
The global impact of Alzheimer's disease (AD) is significant. The current prevalence of Major Neurocognitive Disorder is estimated to affect approximately 44 million individuals. Presently, the United States harbors a population of approximately 6.2 million individuals who are afflicted by Alzheimer's disease (AD) dementia. It is of significance to highlight that mortality associated with Alzheimer's disease (AD) exceeds the combined mortality rates of both breast cancer and prostate cancer. Based on the findings of the National Institute on Aging, the frequency of Alzheimer's disease (AD) exhibits a twofold rise every five years subsequent to attaining the age of 65. Furthermore, with the ongoing process of population aging, an increasingly substantial portion of the population is affected by this particular condition. Based on forecasts, it is anticipated that the United States will experience a financial impact of $355 billion in 2021 as a result of Alzheimer's disease (AD).
Furthermore, same projections indicate that this amount is expected to increase significantly to over $1.5 trillion by the year 2050. As a result, this would place a significant financial strain on the country. Alzheimer's disease (AD) is a neurodegenerative condition that is distinguished by the existence of extracellular amyloid β (Aβ) plaques and intracellular neurofibrillary tangles consisting of hyperphosphorylated τ-protein. The aforementioned abnormal characteristics primarily present themselves inside the cortical and limbic regions of the human brain. The aforementioned ailment is characterized by the presence of memory impairment and a progressive deterioration of neurocognitive abilities. The atypical division of amyloid precursor protein (APP) by β-secretases and γ-secretases leads to the production of Aβ40 and Aβ42 individual molecules, which then undergo the process of oligomerization and aggregation, finally culminating in the formation of senile plaques. The aforementioned disease is additionally aggravated by pathogenic microorganisms, including the human immunodeficiency virus (HIV).
Moreover, within the framework of disease pathophysiology, the presence of heightened amounts of Aβ peptides within the central nervous system induces the infiltration of microglial cells. Presently, there exists a notable focus within the realm of scientific inquiry on gaining a comprehensive understanding of the pathological nature of Alzheimer's disease (AD) by means of exploring diverse pathways.
These mechanisms include the abnormal metabolism of tau proteins, the presence of β-amyloid, the inflammatory response, as well as the damage caused by cholinergic dysfunction and free radicals. The ultimate objective of this research is to develop efficacious treatments that can effectively halt or alter the progression of AD. The present study provides an analysis of the pathophysiological mechanisms underlying Alzheimer's disease, as well as an examination of the diagnostic methods employed in its identification. Furthermore, the review explores the many therapy modalities now utilized in managing this neurodegenerative disorder.
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