title: The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: replication in schizophrenia and extension to bipolar disorder with psychosis.
abstract: While microarray studies are generating novel insights into the etiology of major psychiatric disorders, the validation of microarray-identified candidate genes and their role in the causality of these disorders has been less often studied. We have previously demonstrated, by microarray, up-regulation of SELENBP1 in the brain and blood of patients with schizophrenia. The main aim of the current study was to validate this finding using quantitative real-time PCR (QPCR) in an independent brain cohort that included patients with bipolar disorder. Our sample consisted of mRNAs from the dorsolateral prefrontal cortex (dlPFC) of 34 schizophrenic patients, 33 bipolar disorder patients (including 20 with psychotic history), and 34 normal control subjects. QPCR was employed to assess gene expression changes, with C(T) values analyzed using an ANCOVA approach. The results demonstrated that SELENBP1 mRNA was upregulated in schizophrenic brains versus controls (P = 0.046) and, in addition, that SELENBP1 gene expression was strongly positively correlated with presence of psychosis across diagnoses (P < 0.001, increased by 12%). Based on these findings, we conclude that elevated SELENBP1 is a possibly consistent feature in the schizophrenic brain and that this finding could underlie some commonalities of psychosis across the boundaries of diagnoses. Future studies should exploit DNA-based methods and molecular investigations on the role of SELENBP1 in order to gain insights into the nature of its influence on schizophrenia and psychotic symptoms.
authors.affiliation: Department of Psychiatry, University of California, San Diego, La Jolla, California 92093-0603, USA.
authors.forename: Tetsufumi
authors.initials: T
authors.lastname: Kanazawa
authors.forename: Gursharan
authors.initials: G
authors.lastname: Chana
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Glatt
authors.forename: Hideya
authors.initials: H
authors.lastname: Mizuno
authors.forename: Eliezer
authors.initials: E
authors.lastname: Masliah
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yoneda
authors.forename: Ming T
authors.initials: MT
authors.lastname: Tsuang
authors.forename: Ian P
authors.initials: IP
authors.lastname: Everall
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D001714:Bipolar Disorder / Q000235:genetics* / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D015870:Gene Expression / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D011618:Psychotic Disorders / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012559:Schizophrenia / Q000235:genetics* / Q000378:metabolism; D051137:Selenium-Binding Proteins / Q000235:genetics* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D012333:RNA, Messenger; C495175:SELENBP1 protein, human; D051137:Selenium-Binding Proteins