Author:
Lopatko Lindman Karin,Jonsson Caroline,Weidung Bodil,Olsson Jan,Pandey Janardan P.,Prokopenko Dmitry,Tanzi Rudolph E.,Hallmans Göran,Eriksson Sture,Elgh Fredrik,Lövheim Hugo
Abstract
AbstractPILRA (rs1859788 A > G) has been suggested to be a protective variant for Alzheimer’s disease (AD) and is an entry co-receptor for herpes simplex virus-1. We conducted a nested case–control study of 360 1:1-matched AD subjects. Interactions between the PILRA-A allele, APOE risk variants (ε3/ε4 or ε4/ε4) and GM17 for AD risk were modelled. The associations were cross-validated using two independent whole-genome sequencing datasets. We found negative interactions between PILRA-A and GM17 (OR 0.72, 95% CI 0.52–1.00) and between PILRA-A and APOE risk variants (OR 0.56, 95% CI 0.32–0.98) in the discovery dataset. In the replication cohort, a joint effect of PILRA and PILRA × GM 17/17 was observed for the risk of developing AD (p .02). Here, we report a negative effect modification by PILRA on APOE and GM17 high-risk variants for future AD risk in two independent datasets. This highlights the complex genetics of AD.
Funder
the Kempe Foundation
the Swedish Dementia Association
Cure Alzheimer’s Fund
Region Västerbotten
Wallenberg Centre for Molecular Medicine in Umeå
the Swedish Medical Association
the Swedish Alzheimer Fund
Umeå University
Umea University
Publisher
Springer Science and Business Media LLC
Cited by
3 articles.
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