PILRA polymorphism modifies the effect of APOE4 and GM17 on Alzheimer’s disease risk

PILRA (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...

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Published in:Scientific reports 2022-08, Vol.12 (1), p.13264-13264, Article 13264
Main Authors: 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
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Subjects:
631/208
692/699
692/699/375
Alleles
Alzheimer Disease - genetics
Alzheimer's disease
Apolipoprotein E
Apolipoprotein E4 - genetics
Apolipoproteins
Apolipoproteins E - genetics
Case-Control Studies
Chromosomes
Confidence intervals
Datasets
Genes
Genetics
Genomes
Genotype
Genotype & phenotype
Geriatrics
Glycoproteins
Health risk assessment
Health risks
Herpes simplex
Herpes viruses
Humanities and Social Sciences
Humans
Immunoglobulins
Infections
Medicine
Membrane Glycoproteins - genetics
multidisciplinary
Neurodegenerative diseases
Polymorphism
Polymorphism, Genetic
Public health
Receptors, Immunologic - genetics
Science
Science (multidisciplinary)
Whole genome sequencing
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creator Lopatko Lindman, Karin
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Eriksson, Sture
Elgh, Fredrik
Lövheim, Hugo
description PILRA (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 GM 17 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 GM 17 (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 GM 17 high-risk variants for future AD risk in two independent datasets. This highlights the complex genetics of AD.
doi_str_mv 10.1038/s41598-022-17058-6
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subjects 631/208
692/699
692/699/375
Alleles
Alzheimer Disease - genetics
Alzheimer's disease
Apolipoprotein E
Apolipoprotein E4 - genetics
Apolipoproteins
Apolipoproteins E - genetics
Case-Control Studies
Chromosomes
Confidence intervals
Datasets
Genes
Genetics
Genomes
Genotype
Genotype & phenotype
Geriatrics
Glycoproteins
Health risk assessment
Health risks
Herpes simplex
Herpes viruses
Humanities and Social Sciences
Humans
Immunoglobulins
Infections
Medicine
Membrane Glycoproteins - genetics
multidisciplinary
Neurodegenerative diseases
Polymorphism
Polymorphism, Genetic
Public health
Receptors, Immunologic - genetics
Science
Science (multidisciplinary)
Whole genome sequencing
title PILRA polymorphism modifies the effect of APOE4 and GM17 on Alzheimer’s disease risk
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