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Lopatko Lindman, Karin
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Lopatko Lindman, K., Weidung, B., Olsson, J., Josefsson, M., Kok, E., Johansson, A., . . . Lövheim, H. (2019). A genetic signature including apolipoprotein Eε4 potentiates the risk of herpes simplex-associated Alzheimer's disease. Alzheimer's & dementia, 5, 697-704
Open this publication in new window or tab >>A genetic signature including apolipoprotein Eε4 potentiates the risk of herpes simplex-associated Alzheimer's disease
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2019 (English)In: Alzheimer's & dementia, ISSN 1552-5279, Vol. 5, p. 697-704Article in journal (Refereed) Published
Abstract [en]

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). APOE 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 APOEε4 heterozygosity (APOEε24 or ε3/ε4) 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 APOEε4 allele and other AD genetic risk factors might potentiate the risk of HSV1-associated AD.

Keywords
APOEε4, Alzheimer's disease, Apolipoprotein E4, Dementia, HSV, Herpes simplex, Nested case-control study
National Category
Clinical Medicine
Research subject
Medical Virology
Identifiers
urn:nbn:se:umu:diva-167226 (URN)10.1016/j.trci.2019.09.014 (DOI)31921962 (PubMedID)
Available from: 2020-01-13 Created: 2020-01-13 Last updated: 2020-01-14Bibliographically approved
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