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A genome-wide association study in multiple system atrophy. | LitMetric

AI Article Synopsis

  • The study aimed to discover genetic variants involved in multiple system atrophy (MSA) through a genome-wide association study (GWAS) involving over 900 patients and nearly 4,000 controls.
  • Despite analyzing more than 5 million genetic markers, the researchers found no significant genetic loci linked to MSA after rigorous statistical testing, though some regions showed potential for further investigation.
  • Notably, the study did not find associations between MSA and genes previously implicated in the condition (SNCA and COQ2), and emphasized the need for larger sample sizes in future research to confirm initial findings.

Article Abstract

Objective: To identify genetic variants that play a role in the pathogenesis of multiple system atrophy (MSA), we undertook a genome-wide association study (GWAS).

Methods: We performed a GWAS with >5 million genotyped and imputed single nucleotide polymorphisms (SNPs) in 918 patients with MSA of European ancestry and 3,864 controls. MSA cases were collected from North American and European centers, one third of which were neuropathologically confirmed.

Results: We found no significant loci after stringent multiple testing correction. A number of regions emerged as potentially interesting for follow-up at p < 1 × 10, including SNPs in the genes FBXO47, ELOVL7, EDN1, and MAPT. Contrary to previous reports, we found no association of the genes SNCA and COQ2 with MSA.

Conclusions: We present a GWAS in MSA. We have identified several potentially interesting gene loci, including the MAPT locus, whose significance will have to be evaluated in a larger sample set. Common genetic variation in SNCA and COQ2 does not seem to be associated with MSA. In the future, additional samples of well-characterized patients with MSA will need to be collected to perform a larger MSA GWAS, but this initial study forms the basis for these next steps.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067544PMC
http://dx.doi.org/10.1212/WNL.0000000000003221DOI Listing

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