Role of Selenium and Other Trace Elements in the Geography of Schizophrenia

Brown, James S.

doi:10.1093/schbul/20.2.387

Cited by 35 publications

(12 citation statements)

References 65 publications

(67 reference statements)

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“…Apart from its role in binding selenium, it has been localized to the golgi apparatus, is localized to the growing tips of neurons, and has been associated with ovarian cancer [Huang et al, 2006]. An epidemiological study has shown that regions of the United States with selenium deficiency in the soil are associated with higher frequencies of schizophrenia [Brown, 1994], and other studies have demonstrated that selenium deficiency can directly regulate glutamate-induced oxidative stress in the brain [Ramaekers et al, 1994;Savaskan et al, 2003]. Although such disparate findings still preclude us from advancing a unifying theory on the role of SELENBP1 in psychosis, they do generate interesting empirical questions for future work.…”

Section: Discussionmentioning

confidence: 99%

The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: Replication in schizophrenia and extension to bipolar disorder with psychosis

Kanazawa

Chana

Glatt

et al. 2008

American J of Med Genetics Pt B

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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.

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Section: Discussionmentioning

confidence: 99%

The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: Replication in schizophrenia and extension to bipolar disorder with psychosis

Kanazawa

Chana

Glatt

et al. 2008

American J of Med Genetics Pt B

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“…Thus, the up‐regulation of SEPX1 may play a role in the pathophysiology of schizophrenia. Geographical analysis showed that low selenium in soil and food might be associated with schizophrenia [Brown, 1994]. At deficiency selenium is preferentially retained in the brain compared with other organs, and several studies have shown that selenium deficiency is associated with mood [Benton, 2002].…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation ofADMandSEPX1in the lymphoblastoid cells of patients in monozygotic twins discordant for schizophrenia

Kakiuchi

Ishiwata

Nanko

et al. 2007

American J of Med Genetics Pt B

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The contribution of genetic factors to schizophrenia is well established and recent studies have indicated several strong candidate genes. However, the pathophysiology of schizophrenia has not been totally elucidated yet. To date, studies of monozygotic twins discordant for schizophrenia have provided insight into the pathophysiology of this illness; this type of study can exclude inter-individual variability and confounding factors such as effects of drugs. In this study we used DNA microarray analysis to examine the mRNA expression patterns in the lymphoblastoid (LB) cells derived from two pairs of monozygotic twins discordant for schizophrenia. From five independent replicates for each pair of twins, we selected five genes, which included adrenomedullin (ADM) and selenoprotein X1 (SEPX1), as significantly changed in both twins with schizophrenia. Interestingly, ADM was previously reported to be up-regulated in both the LB cells and plasma of schizophrenic patients, and SEPX1 was included in the list of genes up-regulated in the peripheral blood cells of schizophrenia patients by microarray analysis. Then, we performed a genetic association study of schizophrenia in the Japanese population and examined the copy number variations, but observed no association. These findings suggest the possible role of ADM and SEPX1 as biomarkers of schizophrenia. The results also support the usefulness of gene expression analysis in LB cells of monozygotic twins discordant for an illness.

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“…Deficiencies of heavy the time of conception, and Templer et al (1978), who reported ''a rather consistent trend of schizometals such as magnesium ( Yassa et al, 1979), zinc (Andrews, 1990), and selenium (Foster, 1988; phrenics being born in cold months and conceived in warm months ''. McNeil et al (1975), studying Berry, 1994;Brown, 1994) have been reported to cause schizophrenia-like syndromes. Similarly, a sample of 13 440 individuals with schizophrenia in Sweden, was unable to corroborate an associaexposure to industrial chemicals, such as toluene, is also known occasionally to cause schizophreniation between summer temperatures at the time of conception and winter births of individuals with like syndromes (Goldbloom and Chouinard, 1985).…”

Section: Seasonal Variation In External Toxins 89 Temperature and Wmentioning

confidence: 99%

Seasonality of births in schizophrenia and bipolar disorder: a review of the literature

Torrey

Miller

Rawlings

et al. 1997

Schizophrenia Research

577

381

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More than 250 studies, covering 29 Northern and five Southern Hemisphere countries, have been published on the birth seasonality of individuals who develop schizophrenia and/or bipolar disorder. Despite methodological problems, the studies are remarkably consistent in showing a 5-8% winter-spring excess of births for both schizophrenia and mania/bipolar disorder. This seasonal birth excess is also found in schizoaffective disorder (December-March), major depression (March-May), and autism (March) but not in other psychiatric conditions with the possible exceptions of eating disorders and antisocial personality disorder. The seasonal birth pattern also may shift over time. Attempts to correlate the seasonal birth excess with specific features of schizophrenia suggest that winter-spring births are probably related to urban births and to a negative family history. Possible correlations include lesser severity of illness and neurophysiological measures. There appears to be no correlation with gender, social class, race, measurable pregnancy and birth complications, clinical subtypes, or neurological, neuropsychological, or neuroimaging measures. Virtually no correlation studies have been done for bipolar disorder. Regarding the cause of the birth seasonality, statistical artifact and parental procreational habits are unlikely explanations. Seasonal effects of genes, subtle pregnancy and birth complications, light and internal chemistry, toxins, nutrition, temperature/weather, and infectious agents or a combination of these are all viable possibilities. © 1997 Elsevier Science B.V.

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Role of Selenium and Other Trace Elements in the Geography of Schizophrenia

Cited by 35 publications

References 65 publications

The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: Replication in schizophrenia and extension to bipolar disorder with psychosis

The utility of SELENBP1 gene expression as a biomarker for major psychotic disorders: Replication in schizophrenia and extension to bipolar disorder with psychosis

Up‐regulation ofADMandSEPX1in the lymphoblastoid cells of patients in monozygotic twins discordant for schizophrenia

Seasonality of births in schizophrenia and bipolar disorder: a review of the literature

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