{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T12:44:25Z","timestamp":1781009065537,"version":"3.54.1"},"reference-count":66,"publisher":"Cambridge University Press (CUP)","issue":"4","license":[{"start":{"date-parts":[[2013,6,24]],"date-time":"2013-06-24T00:00:00Z","timestamp":1372032000000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Psychol. Med."],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:sec id=\"S0033291713001414_sec_a1\"><jats:title>Background<\/jats:title><jats:p>Recent studies have provided strong evidence that variation in the gene neurocan (<jats:italic>NCAN<\/jats:italic>, rs1064395) is a common risk factor for bipolar disorder (BD) and schizophrenia. However, the possible relevance of<jats:italic>NCAN<\/jats:italic>variation to disease mechanisms in the human brain has not yet been explored. Thus, to identify a putative pathomechanism, we tested whether the risk allele has an influence on cortical thickness and folding in a well-characterized sample of patients with schizophrenia and healthy controls.<\/jats:p><\/jats:sec><jats:sec id=\"S0033291713001414_sec_a2\" sec-type=\"methods\"><jats:title>Method<\/jats:title><jats:p>Sixty-three patients and 65 controls underwent T1-weighted magnetic resonance imaging (MRI) and were genotyped for the single nucleotide polymorphism (SNP) rs1064395. Folding and thickness were analysed on a node-by-node basis using a surface-based approach (FreeSurfer).<\/jats:p><\/jats:sec><jats:sec id=\"S0033291713001414_sec_a3\" sec-type=\"results\"><jats:title>Results<\/jats:title><jats:p>In patients,<jats:italic>NCAN<\/jats:italic>risk status (defined by AA and AG carriers) was found to be associated with higher folding in the right lateral occipital region and at a trend level for the left dorsolateral prefrontal cortex. Controls did not show any association (<jats:italic>p<\/jats:italic>\u00a0&gt;\u00a00.05). For cortical thickness, there was no significant effect in either patients or controls.<\/jats:p><\/jats:sec><jats:sec id=\"S0033291713001414_sec_a4\" sec-type=\"conclusion\"><jats:title>Conclusions<\/jats:title><jats:p>This study is the first to describe an effect of the<jats:italic>NCAN<\/jats:italic>risk variant on brain structure. Our data show that the<jats:italic>NCAN<\/jats:italic>risk allele influences cortical folding in the occipital and prefrontal cortex, which may establish disease susceptibility during neurodevelopment. The findings suggest that<jats:italic>NCAN<\/jats:italic>is involved in visual processing and top-down cognitive functioning. Both major cognitive processes are known to be disturbed in schizophrenia. Moreover, our study reveals new evidence for a specific genetic influence on local cortical folding in schizophrenia.<\/jats:p><\/jats:sec>","DOI":"10.1017\/s0033291713001414","type":"journal-article","created":{"date-parts":[[2013,6,24]],"date-time":"2013-06-24T12:32:23Z","timestamp":1372077143000},"page":"811-820","source":"Crossref","is-referenced-by-count":54,"title":["Common variation in<i>NCAN<\/i>, a risk factor for bipolar disorder and schizophrenia, influences local cortical folding in schizophrenia"],"prefix":"10.1017","volume":"44","author":[{"given":"C. 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