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Clinical onset of amyotrophic lateral sclerosis (ALS) is a complex multifactorial process that is only partially explained by inherited genetic variants. Recent GWASs have found several other risk loci, but there are no candidate genes or biological mechanisms explaining their association with ALS. In this study, we propose that the risk variants identified by GWAS could be associated with NMDARs, the glutamate receptors mediating excitatory neurotransmission.
Materials and methods
We searched for available eQTL, exome and genome data for the GWAS risk loci and correlated them with the occurrence of ALS cases and controls in the ALS Genetic database, in the ALS Genetic database, in the 1000 Genomes project, and in the ESP6500 exome project.
We found that three of the risk loci reported in the ALS GWAS are significantly correlated (r^2^ > 0.6) with splicing variants of the NMDAR1 and NMDAR3 genes located on