A genetic signature including apolipoprotein E?4 potentiates the risk of herpes simplex-associated Alzheimer's disease.

ABSTRACT: Introduction:Herpes simplex virus type 1 (HSV1) in combination with genetic susceptibility has previously been implicated in Alzheimer's disease (AD) pathogenesis. Methods:Plasma from 360 AD cases, obtained on average 9.6 years before diagnosis, and their age- and sex-matched controls, were analyzed for anti-HSV1 immunoglobulin (Ig) G with enzyme-linked immunosorbent assays (ELISAs). A POE genotype and nine other selected risk genes for AD were extracted from a genome-wide association study analysis by deCODE genetics, Reykjavik, Iceland. Results:The interaction between APOE?4 heterozygosity (APOE?2/?4 or ?3/?4) and anti-HSV1 IgG carriage increased the risk of AD (OR 4.55, P = .02). A genetic risk score based on the nine AD risk genes also interacted with anti-HSV1 IgG for the risk of developing AD (OR 2.35, P = .01). Discussion:The present findings suggest that the APOE?4 allele and other AD genetic risk factors might potentiate the risk of HSV1-associated AD.

SUBMITTER: Lopatko Lindman K 

PROVIDER: S-EPMC6944738 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature