| Literature DB >> 34183866 |
Gerald Nestadt1, David B Goldstein2, Mathew Halvorsen3, Jack Samuels4, Ying Wang5, Benjamin D Greenberg6, Abby J Fyer7, James T McCracken8, Daniel A Geller9, James A Knowles10, Anthony W Zoghbi7,11, Tess D Pottinger11, Marco A Grados4, Mark A Riddle4, O Joseph Bienvenu4, Paul S Nestadt4, Janice Krasnow4, Fernando S Goes4, Brion Maher12.
Abstract
Obsessive-compulsive disorder (OCD) affects 1-2% of the population, and, as with other complex neuropsychiatric disorders, it is thought that rare variation contributes to its genetic risk. In this study, we performed exome sequencing in the largest OCD cohort to date (1,313 total cases, consisting of 587 trios, 41 quartets and 644 singletons of affected individuals) and describe contributions to disease risk from rare damaging coding variants. In case-control analyses (n = 1,263/11,580), the most significant single-gene result was observed in SLITRK5 (odds ratio (OR) = 8.8, 95% confidence interval 3.4-22.5, P = 2.3 × 10-6). Across the exome, there was an excess of loss of function (LoF) variation specifically within genes that are LoF-intolerant (OR = 1.33, P = 0.01). In an analysis of trios, we observed an excess of de novo missense predicted damaging variants relative to controls (OR = 1.22, P = 0.02), alongside an excess of de novo LoF mutations in LoF-intolerant genes (OR = 2.55, P = 7.33 × 10-3). These data support a contribution of rare coding variants to OCD genetic risk.Entities:
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Year: 2021 PMID: 34183866 DOI: 10.1038/s41593-021-00876-8
Source DB: PubMed Journal: Nat Neurosci ISSN: 1097-6256 Impact factor: 24.884