Alzheimer’s disease (AD) is a neurodegenerative disease characterized by
the progressive loss of cognitive functions in affected individuals. Brain
tissue pathology is associated with the formation of senile plaques which
result from the over-production of amyloid β (Aβ), due to the cleavage of a
membrane bound glycoprotein. It is unclear what causes AD and its associated
pathologies, but age and genetic predisposition play an import role in the
likelihood of disease development. Studies have shown that the reactivation of
latent herpes simplex virus 1 (HSV-1) infection can lead to the neuropathy of
acute herpes simplex encephalitis (HSE), which causes similar symptoms to AD.
HSV-1 infection is a known risk factor for the development of AD, but no study
has determined a definitive causal relationship. Using the Qiagen Ingenuity Pathway Analysis (IPA) tool, the
inhibitory relationship between therapeutics for AD and HSV-1 were
explored. Thirteen drugs developed to decrease Aβ buildup in AD and 32 drugs that act as HSV antivirals were
retrieved from the data in the Qiagen Knowledge Base. These drugs were analyzed
displayed as two separate networks. While many promising Aβ aggregation-targeting drugs have been discontinued due to lack of
efficacy, HSV drugs could serve as potential therapeutics for those with AD.
This review aims to describe new insights on how HSV-1 relates to the
development of AD and highlight the mechanism of action of Aβ-related drugs and HSV drugs in the
context of AD. With HSV-1 being a likely candidate for the causation of AD,
there is a need to study the effects of HSV antiviral drugs on those who have
AD.
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