Alzheimer’s Disease Pathogenesis and Herpes Simplex Virus

Abstract

Alzheimer's disease is a disease of the central nervous system for which there is currently no cure. Over the years researchers have postulated many theories and hypotheses about the causative agents of the disease. The disease is suggested to be a result of a combination of multiple environmental, pathogenic(viral), lifestyle and genetic factors. It is hallmarked by the presence of plaques and tangles in the brain which lead neuronal degeneration symptomized by decline in cognitive abilities, behavioral impedance, inability to perform simple daily tasks, and in some cases impairment of sight and smell. Particularly, Herpes Simplex Virus 1 has been one of the most widely studied viral factors in connection to Alzheimer's disease pathogenesis. For the purpose of this paper, I propose that Herpes Simplex Virus 1 is a major contributor to the series of neuronal processes that lead to the generation of plaques and tangles in the brain, and thus it may provide a new approach towards finding a cure for Alzheimer's disease.

Introduction

Alzheimer's disease (AD) is a neurodegenerative disease which presents more prevalently in older adults and has a wide variety of probable causative agents, age being one of the most common. In 2000, there were 4.5 million persons with AD in the US population. By 2050, this number will increase by almost 3-fold, to 13.2 million (Herbert et al., 2003). This proposed increase in the number of people with Alzheimer's by the year 2050 is a result of the rapid increase in the number of the aging population in the United states. Alzheimer's disease, like any other disease, is detrimental to the health and lifestyle of affected individuals. Thedisease is characterized by progressive decline in cognitive abilities, behavioral abnormalities, and the loss of ability to function at work or in activities of daily living (Harris and Harris, 2018). Research's over the years have continued to link a wide number of factors as contributing agents towards the occurrence and progression of AD. From genetics to lifestyle, the number of factors that contribute to the development of Alzheimer's later or early in life is exhaustive. A higher percentage of diagnosis of Alzheimer's occur at a later stage of life but as with all things, there exists an exception to this norm.

A small percentage of the Alzheimer's presenting population are diagnosed at an earlier age than usual. Early-onset Alzheimer's disease (EOAD), as it is termed,accounts for 16% of all cases and ranges approximately with onset from 30“60 or 65 years (Alonso Vilatela et al., 2012). About 60% of these patients are classified as familial EOAD, having multiple relatives diagnosed with the disease (Harris and Harris, 2018). The familial nature of EOAD is linked to a genetic mutation in families with this form of AD. According to Betram and Tanzi (2008),all mutations that are currently known to cause AD in early­-onset autosomal dominant families are located either in the amyloid precursor protein (APP)gene itself or in the genes that encode the proteins that lie at the catalytic center of the-secretase complex: presenilin 1 (PSEN1) and presenilin 2 (PSEN2).

By contrast, suscep­tibility for late­-onset AD (> 60 or 65 years) shows less? obvious or no appar­ent familial aggregation (hence it is sometimes called 'sporadic' AD) and is likely to be governed by an array of common risk alleles across a number of different genes (Betram and Tanzi, 2008). Both forms of Alzheimer's appear to be linked to a genetic factor, with the EOAD being more specific to a particular gene locus and the LOAD linked to a number of genes. Nonetheless, both forms of AD are influenced by factors other than genetics which eventually leads to the manifestation of the disease early or later on. Some of these other factors that lead to onset of Alzheimer's are cerebrovascular accidents mostly due to falls, stress, immunosuppression, strokes, viral infections etc. For the purpose of this paper, the possible correlation between viral infections of the brain, specifically Herpes Simplex Virus 1, and the pathogenesis of AD will be analyzed.

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