Abstract
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.
Highlights
Dementia is described as the overall decline in the ability to cognitively function due to a disease or debilitating condition
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 Alzheimer’s disease (AD)
AD is a complicated disease due to the number of factors that have been suggested to be a part of the pathology and the notable length of time it takes for symptoms to manifest
Summary
Dementia is described as the overall decline in the ability to cognitively function due to a disease or debilitating condition. Alzheimer’s disease (AD) is the leading cause of dementia and it is estimated that 60% - 80% of the 45 million individuals diagnosed with dementia have AD [2]. This neurodegenerative decline is characterized by a widespread shrinkage of brain mass due to the loss of neurons and their respective dendritic connections. There are only two FDA-approved classes of AD drugs, which are cholinesterase inhibitors and the N-methyl-D-aspartate (NMDA) receptor antagonist memantine. Memantine is a noncompetitive antagonist of the NMDA receptor that functionally blocks the flow of ions and in AD can slightly improve memory and cognitive function. By exploring the molecular pathology and potential cause(s) of AD, a better appreciation and thorough understanding of this disease are attainable, resulting in the path forward to more impactful drug therapies
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