文献类型：期刊文献

英文题名：Independent and Correlated Role of Apolipoprotein E epsilon 4 Genotype and Herpes Simplex Virus Type 1 in Alzheimer's Disease

作者：Zhang, Li-Na[1,2,3];Li, Meng-Jie[1,2,3];Shang, Ying-Hui[1,2,3];Zhao, Fan-Fan[1,2,3];Huang, Han-Chang[1,2,3];Lao, Feng-Xue[1,2,3]

通讯作者：Lao, FX[1];Lao, FX[2];Lao, FX[3]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing 100191, Peoples R China;[3]Beijing Union Univ, Coll Biochem Engn, Beijing 100191, Peoples R China

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]corresponding author), Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing 100191, Peoples R China;[3]corresponding author), Beijing Union Univ, Coll Biochem Engn, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2020

卷号：77

期号：1

起止页码：15-31

外文期刊名：JOURNAL OF ALZHEIMERS DISEASE

收录：;Scopus(收录号：2-s2.0-85090510412);WOS:【SCI-EXPANDED(收录号:WOS:000568816600002)】；

基金：Financial support from the National Natural Science Foundation of China (31471587), Ten Frontier Research Directions of Discipline Orientation (ZK40201902) and Graduate Funding Project of Beijing Union University are gratefully acknowledged.

语种：英文

外文关键词：Alzheimer's disease; apolipoprotein E; cytokine; estrogen therapy; herpes simplex virus type 1; infectious burden; interferon

摘要：The 84 allele of the Apolipoprotein E (APOE) gene in individuals infected by Herpes simplex virus type 1 (HSV-1) has been demonstrated to be a risk factor in Alzheimer's disease (AD). APOE-84 reduces the levels of neuronal cholesterol, interferes with the transportation of cholesterol, impairs repair of synapses, decreases the clearance of neurotoxic peptide amyloid-P (AP), and promotes the deposition of amyloid plaque, and eventually may cause development of AD. HSV-1 enters host cells and can infect the olfactory system, trigeminal ganglia, entorhinal cortex, and hippocampus, and may cause AD-like pathological changes. The lifecycle of HSV-1 goes through a long latent phase. HSV-1 induces neurotropic cytokine expression with pro-inflammatory action and inhibits antiviral cytokine production in AD. It should be noted that interferons display antiviral activity in HSV-1-infected AD patients. Reactivated HSV-1 is associated with infectious burden in cognitive decline and AD. Finally, HSV-1 DNA has been confirmed as present in human brains and is associated with APOE 84 in AD. HSV-1 and APOE 84 increase the risk of AD and relate to abnormal autophagy, higher concentrations of HSV-1 DNA in AD, and formation of AP plaques and neurofibrillary tangles.