{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T19:14:13Z","timestamp":1788462853624,"version":"build-2803163510"},"reference-count":57,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T00:00:00Z","timestamp":1345593600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J of Med Genetics Pt B"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Panic disorder (PD) is a common mental disorder, ranking highest among the anxiety disorders in terms of disease burden. The pathogenesis of PD is multifactorial with significant heritability, however only a few convincing risk genes have been reported thus far. One of the most promising candidates is the gene encoding monoamine oxidase A (<jats:italic>MAOA<\/jats:italic>), due to its key role in monoaminergic neurotransmission, established validity of animal models, and the efficacy of MAO inhibitors in the treatment of PD. A promoter repeat polymorphism in<jats:italic>MAOA<\/jats:italic>(<jats:italic>MAOA<\/jats:italic>\u2010uVNTR) impacts on gene expression; high\u2010expression alleles have been reported to increase the risk for PD. To further scrutinize the role of this polymorphism, we performed a formal meta\u2010analysis on<jats:italic>MAOA<\/jats:italic>\u2010uVNTR and PD using original data from four published European (Estonian, German, Italian, and Polish) samples and genotypes from three hitherto unpublished German PD samples, resulting in the largest (n\u2009=\u20091,115 patients and n\u2009=\u20091,260 controls) genetic study on PD reported to date. In the unpublished samples, evidence for association of<jats:italic>MAOA<\/jats:italic>\u2010uVNTR with PD was obtained in one of the three samples. Results of the meta\u2010analysis revealed a significant and female\u2010specific association when calculating an allelic model (OR\u2009=\u20091.23,<jats:italic>P<\/jats:italic>\u2009=\u20090.006). This sex\u2010specific effect might be explained by a gene\u2010dose effect causing higher<jats:italic>MAOA<\/jats:italic>expression in females. Taken together, our meta\u2010analysis therefore argues that high\u2010expression<jats:italic>MAOA<\/jats:italic>\u2010uVNTR alleles significantly increase the risk towards PD in women. However, epigenetic mechanisms might obfuscate the genetic association, calling for ascertainment in larger samples as well as assessment of the<jats:italic>MAOA<\/jats:italic>promoter methylation status therein. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/ajmg.b.32085","type":"journal-article","created":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T12:09:31Z","timestamp":1345637371000},"page":"786-793","source":"Crossref","is-referenced-by-count":61,"title":["Meta\u2010analysis argues for a female\u2010specific role of<i>MAOA<\/i>\u2010uVNTR in panic disorder in four European 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