Selenium and neurological diseases
Type of Spiritual Experience
Selenium-binding protein 1 is a protein that in humans is encoded by the SELENBP1 gene.
This gene product belongs to the selenium-binding protein family. Selenium is an essential nutrient that exhibits potent anticarcinogenic properties, and deficiency of selenium may cause certain neurologic diseases. It has been proposed that the effects of selenium in preventing neurologic diseases may be mediated by selenium-binding proteins. The exact function of this gene is not yet known.
Please note that the paper does not imply one should dose oneself up on selenium, it implies that if there is imbalance, then neurological diseases may result
A description of the experience
Am J Med Genet B Neuropsychiatr Genet. 2008 Sep 5;147B(6):686-9. doi: 10.1002/ajmg.b.30664.
The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: replication in schizophrenia and extension to bipolar disorder with psychosis.
Kanazawa T1, Chana G, Glatt SJ, Mizuno H, Masliah E, Yoneda H, Tsuang MT, Everall IP. 1Department of Psychiatry, University of California, San Diego, La Jolla, California 92093-0603, USA.
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.
2007 Wiley-Liss, Inc.