| Literature DB >> 35156446 |
Lincoln Mp Shade1, Yuriko Katsumata1,2, Timothy J Hohman3, Kwangsik Nho4, Andrew J Saykin4, Shubhabrata Mukherjee5, Kevin L Boehme6, John Sk Kauwe7, Lindsay A Farrer8, Gerard D Schellenberg9, Jonathan L Haines10, Richard P Mayeux11, Julie A Schneider12, Peter T Nelson2,13, David W Fardo1,2.
Abstract
Brain arteriolosclerosis (B-ASC) is characterized by pathologically altered brain parenchymal arterioles. B-ASC is associated with cognitive impairment and increased likelihood of clinical dementia. To date, no study has been conducted on genome-wide genetic risk of autopsy-proven B-ASC. We performed a genome-wide association study (GWAS) of the B-ASC phenotype using multiple independent aged neuropathologic cohorts. Included in the study were participants with B-ASC autopsy and genotype data available from the NACC, ROSMAP, ADNI, and ACT data sets. Initial Stage 1 GWAS (n = 3382) and Stage 2 mega-analysis (n = 4569) were performed using data from the two largest cohorts (NACC and ROSMAP). Replication of top variants and additional Stage 3 mega-analysis were performed incorporating two smaller cohorts (ADNI and ACT). Lead variants in the top two loci in the Stage 2 mega-analysis (rs7902929, p = 1.8×10-7; rs2603462, p = 4×10-7) were significant in the ADNI cohort (rs7902929, p = 0.012; rs2603462, p =0.012). The rs2603462 lead variant colocalized with ELOVL4 expression in the cerebellum (posterior probability = 90.1%). Suggestive associations were also found near SORCS1 and SORCS3. We thus identified putative loci associated with B-ASC risk, but additional replication is needed.Entities:
Keywords: SVD; VCID; aging; arteriosclerosis; dementia; neuropathology
Mesh:
Year: 2022 PMID: 35156446 PMCID: PMC9274864 DOI: 10.1177/0271678X211066299
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN: 0271-678X Impact factor: 6.960