Open AccessA genetic signature including apolipoprotein Eε4 potentiates the risk of herpes simplex–associated Alzheimer's disease
Author(s) -
Lopatko Lindman Karin,
Weidung Bodil,
Olsson Jan,
Josefsson Maria,
Kok Eloise,
Johansson Anders,
Eriksson Sture,
Hallmans Göran,
Elgh Fredrik,
Lövheim Hugo
Publication year - 2019
Publication title -
alzheimer's and dementia: translational research and clinical interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.49
H-Index - 30
ISSN - 2352-8737
DOI - 10.1016/j.trci.2019.09.014
Subject(s) - apolipoprotein e , herpes simplex virus , allele , genotype , disease , immunology , loss of heterozygosity , gene , alzheimer's disease , medicine , antibody , genetics , biology , virology , virus
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 APOEε 4 heterozygosity ( APOEε 2 /ε 4 or ε 3/ ε 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 APOEε 4 allele and other AD genetic risk factors might potentiate the risk of HSV1‐associated AD.