A genetic signature including apolipoprotein Eε4 potentiates the risk of herpes simplex-associated Alzheimer's disease Visa övriga samt affilieringar
2019 (Engelska) Ingår i: Alzheimer’s & Dementia: Translational Research & Clinical Interventions, E-ISSN 2352-8737, Vol. 5, s. 697-704Artikel i tidskrift (Refereegranskat) 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). 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.
Ort, förlag, år, upplaga, sidor 2019. Vol. 5, s. 697-704
Nyckelord [en]
APOEε4, Alzheimer's disease, Apolipoprotein E4, Dementia, HSV, Herpes simplex, Nested case-control study
Nationell ämneskategori
Klinisk medicin
Forskningsämne medicinsk virologi
Identifikatorer URN: urn:nbn:se:umu:diva-167226 DOI: 10.1016/j.trci.2019.09.014 ISI: 000737692800074 PubMedID: 31921962 Scopus ID: 2-s2.0-85074268423 OAI: oai:DiVA.org:umu-167226 DiVA, id: diva2:1385098
2020-01-132020-01-132023-09-05 Bibliografiskt granskad