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We hypothesise that part of AN heritability will be attributable to SVs in risk loci identified by GWAS [2], driving or contributing to the signal of strongly associated SNPs via linkage disequilibrium (LD) [7]

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Paradoxically, this post-transcriptional modification contributes to a subsequent decline in synaptophysin protein abundance, which is associated with disrupted motor coordination and impaired cognitive performance in juvenile micee (Zhang et al