Bioinformatics Review of the Role of HSV-1 in Alzheimer’s Disease

• 作者: Arah C. Godbole Brian T. Reiss Cecelia M. McCann Jessica A. Cottrell Julia A. Marut Meade C. Eggleston Sulie L. Chang Tinchun Chu
• 来源期刊: 阿尔茨海默氏病研究进展(英文)
• 学科: 医学
• 关键词: Alzheimer’s Disease Amyloid β Herpes Simplex Virus-1
• 年，卷（期）: 2020,（3）
• 页码范围: 57-75
• 页数: 19页
• 分类号: R74

摘要

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 </span><i><span style="font-family:Verdana;">β</span></i><span style="font-family:Verdana;"> (A</span><i><span style="font-family:Verdana;">β</span></i><span style="font-family:Verdana;">), 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 In</span><span style="font-family:Verdana;">genuity Pathway Analysis (IPA) tool, the inhibitory relationship between therapeutic</span><span style="font-family:Verdana;">s for AD and HSV-1 were explored. Thirteen drugs developed to decrease A</span><i><span style="font-family:Verdana;">β</span></i><span style="font-family:Verdana;"> 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 A</span><i><span style="font-family:Verdana;">β</span></i><span style="font-family:Verdana;"> 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 A</span><i><span style="font-family:Verdana;">β</span></i><span style="font-family:Verdana;">-related drugs and HSV drugs in the con