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We aimed to validate these findings in a new cohort using real-time PCR in Brodmann\u2019s Area (BA) 9, and to determine the disease specificity of increased <jats:italic>SELENBP1<\/jats:italic> expression by measuring <jats:italic>SELENBP1<\/jats:italic> mRNA in subjects with major depressive disorder and bipolar disorder. We then extended the study to include other cortical regions such as BA8 and BA44. <jats:italic>SELENBP1<\/jats:italic> mRNA was higher in BA9 (<jats:italic>P<\/jats:italic>=0.001), BA8 (<jats:italic>P<\/jats:italic>=0.003) and BA44 (<jats:italic>P<\/jats:italic>=0.0007) from subjects with schizophrenia. Conversely, in affective disorders, there was no significant difference in <jats:italic>SELENBP1<\/jats:italic> mRNA in BA9 (<jats:italic>P<\/jats:italic>=0.67), suggesting that the upregulation may be diagnosis specific. Measurement of SELENBP1 protein levels showed that changes in mRNA did not translate to changes in protein. In addition, chronic treatment of rats with antipsychotics did not significantly affect the expression of <jats:italic>Selenbp1<\/jats:italic> in the cortex (<jats:italic>P<\/jats:italic>=0.24). Our data show that elevated SELENBP1 transcript expression is widespread throughout the prefrontal cortex in schizophrenia, and confirm that this change is a consistent feature of schizophrenia and not a simple drug effect.<\/jats:p>","DOI":"10.1038\/tp.2015.108","type":"journal-article","created":{"date-parts":[[2015,8,4]],"date-time":"2015-08-04T13:42:44Z","timestamp":1438695764000},"page":"e615-e615","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["SELENBP1 expression in the prefrontal cortex of subjects with schizophrenia"],"prefix":"10.1038","volume":"5","author":[{"given":"M","family":"Udawela","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T T","family":"Money","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"Neo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M S","family":"Seo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E","family":"Scarr","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B","family":"Dean","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I P","family":"Everall","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2015,8,4]]},"reference":[{"key":"BFtp2015108_CR1","doi-asserted-by":"publisher","first-page":"15533","DOI":"10.1073\/pnas.0507666102","volume":"102","author":"SJ Glatt","year":"2005","unstructured":"Glatt SJ, Everall IP, Kremen WS, Corbeil J, Sasik R, Khanlou N et al. 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