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Carpanini, Sarah M; Harwood, Janet C; Baker, Emily; Torvell, Megan; The Gerad Consortium; Sims, Rebecca; Williams, Julie; Morgan, B Paul
Genes, 03/2021, Letnik: 12, Številka: 3Journal Article
Late-onset Alzheimer's disease (LOAD), the most common cause of dementia, and a huge global health challenge, is a neurodegenerative disease of uncertain aetiology. To deliver effective diagnostics and therapeutics, understanding the molecular basis of the disease is essential. Contemporary large genome-wide association studies (GWAS) have identified over seventy novel genetic susceptibility loci for LOAD. Most are implicated in microglial or inflammatory pathways, bringing inflammation to the fore as a candidate pathological pathway. Among the most significant GWAS hits are three complement genes: , encoding the fluid-phase complement inhibitor clusterin; encoding complement receptor 1 (CR1); and recently, encoding the complement enzyme C1s. Complement activation is a critical driver of inflammation; changes in complement genes may impact risk by altering the inflammatory status in the brain. To assess complement gene association with LOAD risk, we manually created a comprehensive complement gene list and tested these in gene-set analysis with LOAD summary statistics. We confirmed associations of and genes with LOAD but showed no significant associations for the complement gene-set when excluding and . No significant association with other complement genes, including , was seen in the IGAP dataset; however, these may emerge from larger datasets.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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