{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T01:38:44Z","timestamp":1783042724062,"version":"3.54.6"},"reference-count":52,"publisher":"Canadian Science Publishing","issue":"1","license":[{"start":{"date-parts":[[2021,1,1]],"date-time":"2021-01-01T00:00:00Z","timestamp":1609459200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Psychiatry Neurosci"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p> Cumulative exposure to high glucocorticoid levels is detrimental for the brain and may have particular implications in later life. A feature of late-life depression is increased cortisol secretion. Variants in the CYP11B1 gene, which codes for the enzyme responsible for cortisol synthesis, could influence risk of late-life depression, but this hypothesis has not been examined. We investigated the associations between variants in the CYP11B1 gene and late-life depression, taking into account history of depression and potential sex-specific effects. <\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p> We assessed depression in 1007 community-dwellers aged 65 years or older (60% women) at baseline and over a 14-year follow-up. A clinical level of depression was defined as a score of \u2265 16 on the Centre for Epidemiology Studies Depression scale or a diagnosis of current major depression based on the Mini-International Neuropsychiatric Interview and according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). We examined incident and recurrent depression in participants without or with a history of major depression, respectively. We genotyped 5 single-nucleotide polymorphisms (SNPs) spanning CYP11B1. We used multivariable analyses to adjust for age, body mass index, cardiovascular ischemic pathologies, hypertension, cognitive impairment and anxiety. <\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p> In women, rs6471580 and rs7016924 were associated with a 50% lower rate of incident (new-onset) late-life depression, and rs11783855 was associated with a 2.4-fold higher rate of late-life depression. These associations remained after correction for multiple testing, but we found no associations for recurrent depression in women or men. <\/jats:p><\/jats:sec><jats:sec><jats:title>Limitations<\/jats:title><jats:p> This study focused on the major gene involved in corticosteroid biosynthesis, but other genes may also be implicated in this pathway. <\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p> Variants of the CYP11B1 gene appear to be susceptibility factors for late-life depression in a sex-specific manner. <\/jats:p><\/jats:sec>","DOI":"10.1503\/jpn.190177","type":"journal-article","created":{"date-parts":[[2021,1,4]],"date-time":"2021-01-04T08:33:01Z","timestamp":1609749181000},"page":"E147-E153","source":"Crossref","is-referenced-by-count":8,"title":["11\u03b2-Hydroxylase (<i>CYP11B1<\/i>) gene variants and new-onset depression in later 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