Zameel M. Cader

TL;DR: For example, the authors identified 44 independent single-nucleotide polymorphisms (SNPs) significantly associated with migraine risk (P < 5 × 10−8) that mapped to 38 distinct genomic loci, including 28 loci not previously reported and a locus that to date is the first to be identified on chromosome X.

TL;DR: A genome-wide screen of 43 Canadian families, segregating MA with families chosen for an apparent autosomal dominant pattern of transmission revealed a novel locus on 11q24 with a two-point LOD score of 4.2 and a multi-point parametric Lod score of 5.6, powerful evidence that a gene increasing susceptibility to MA resides on this region of the genome.

TL;DR: The functional characterisation of additional TRESK channel missense variants identified in unrelated patients indicates that a single non-functional TResK variant is not alone sufficient to cause typical migraine and highlights the genetic complexity of this disorder.

TL;DR: The overall excess allele sharing observed for the entire sample was due to increased allele sharing within the DRB1*15 negative subgroup alone, which is most consistent with a model of genetic heterogeneity between HLA and other genetic loci.

TL;DR: The largest genetic study of migraine to date, comprising 59,674 cases and 316,078 controls from 22 GWA studies, identified 45 independent single nucleotide polymorphisms significantly associated with migraine risk that map to 38 distinct genomic loci, including 28 loci not previously reported and the first locus identified on chromosome X.