subject: Association Of Hsv And Alzheimers Disease [print this page] An infectious agent or predisposing factor has long been sought for many neurological disorders, including the insidious and debilitating Alzheimers disease (AD). Herpes simplex virus type 1 has been studied extensively as a candidate for an aetiological agent due to its ubiquitous and neurotropic nature, and the similarity of the sites of human brain infection and AD pathologies.
Collectively, current research indicates that HSV-1 infection of the brain, although not the cause of AD, is a significant risk factor, potentially predisposing individuals to increased inflammation, neuritic plaque and neurofibrillary tangle formation and beta-amyloid deposition.
Alois Alzheimer described the salient clinical features of AD in 1907 through a case report of progressive dementia in a psychiatric patient in his care. His patient, Auguste D, probably suffered from many of the classic symptoms of this disease, including memory loss, paranoid and altered behaviours, reduced higher intellectual functions and loss of linguistic ability.
Alzheimers report marked the beginning of almost 100 years of clinical and research effort designed to establish both an understanding of the aetiology of this insidious neurological disorder and the development of a cure. Substantial progress has been made but the search for the causative agents continues.
As a consequence of the investigation into the aetiology of sporadic AD, many risk factors associated with the development of AD have been identified, including age, head injury accompanied by loss of consciousness, and a family history of AD, which suggests the involvement of common environmental factors.
Although they remain controversial, protective factors have been identified also and these include an increased level of education, hormone replacement therapy in women, and the use of anti-inflammatory drugs. Despite these advances in our understanding of the disease, no single causative agent has been established for the more common, sporadic form of AD.
Due to the common and neurological nature of sporadic AD, neurotropic and ubiquitous candidate pathogens were investigated. A prime candidate has been HSV-1, a neurotropic virus that is almost ubiquitous in the human population. HSV-1 also shows a predilection for infection of anatomical sites of the brain that are commonly damaged in AD.
First suggested by Ball in 1982, HSV-1 has since been established as a prominent risk factor for AD. Other pathogens, including herpes virus family members, have been investigated, but currently, HSV-1 is the only infectious agent thought to have a possible association with AD development.
A considerable number of studies have been completed over the past 20 years to assess whether or not the presence of HSV-1 in the aged brain is associated with AD using increasingly more sensitive techniques. Although there are some contradictory findings, by and large, the studies indicate that HSV-1 is found commonly in the brains of individuals who had AD. Greater variability and a lower frequency of HSV-1 detection was found in the earlier studies that employed less sensitive techniques.
With the advent of more sensitive polymerase chain reaction (PCR) techniques, the consistent detection of HSV-1 has indicated a strong correlation between HSV-1 in the brain and AD. The more recent PCR-based studies also indicated that HSV-1 is found at fairly high frequency in normal aged human brain, but is absent from most younger human brain samples examined.
An absence of central nervous system (CNS) infection by another member of the herpes virus family (varicella zoster virus) was also established, supporting the association of HSV-1 with AD. HSV-1, on its own, is not the sole causative agent because AD develops in a subset of those individuals with evidence of CNS infection but it is an established risk factor for AD.
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