Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genome-wide gene expression analysis using DNA microarray has a great advantage to identify the genes or specific molecular cascades involved in mental diseases, including major depression and suicide. In the present study, we conducted DNA microarray analysis of major depression using postmortem prefrontal cortices. The gene expression patterns were compared between the controls and subjects with major depression. As a result, 99 genes were listed as the differentially expressed genes in major depression, of which several genes such as FGFR1, NCAM1, and CAMK2A were of interest. Gene ontology analysis suggested an overrepresentation of genes implicated in the downregulation or inhibition of cell proliferation. The present results may support the hypothesis that major depression is associated with impaired cellular proliferation and plasticity. Comparison between the controls and suicide victims with major depression, bipolar disorder, or schizophrenia was also conducted in the present study. Two genes, CAD and ATP1A3, were differentially expressed in the three comparisons in the same direction. Interestingly, these two genes were also included in the differentially expressed 99 genes in major depression. It may be worth investigating the genes in relation to suicide or major depression.
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PMID:Gene expression profiling of major depression and suicide in the prefrontal cortex of postmortem brains. 1806 48

Despite tremendous efforts of experimental and clinical studies and knowledge, the pathophysiology of severe mental illness (SMI), including bipolar disorder (BD), unipolar depression (mood disorders, MD), and schizophrenia (SCZ), remains poorly understood. Besides their chronic course and high prevalence in society, mental and somatic comorbidities are really serious problems; patients with these disorders have increased risk of cardiovascular (CV) diseases (CVD) including coronary artery diseases (CAD, i.e. myocardial infarction and angina), stroke, sudden cardiac death, hypertension, cardiomyopathy, arrhythmia, and thromboembolic disease. Although it is determined that triglycerides, cholesterol, glucose, and low-density lipoprotein (LDL) levels are increased in MD and SCZ, the underlying reason remains unknown. Considering this, we propose that electronegative LDL (L5) is probably the main crucial element to understanding CVD induced by SMI and to discovering novel remedial approaches for these diseases. When it is hypothesized that L5 is greatly presupposed in CV system abnormalities, it follows that the anti-L5 therapies and even antioxidant treatment options may open new therapeutic opportunities to prevent CVD diseases secondary to SMI. In this review article, we tried to bring a very original subject to the attention of readers who are interested in lipoprotein metabolism in terms of experimental, clinical, and cell culture studies that corroborate the involvement of L5 in physiopathology of CVD secondary to SMI and also the new therapeutic approaches for these disorders.
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PMID:Why are cardiovascular diseases more common among patients with severe mental illness? The potential involvement of electronegative low-density lipoprotein (LDL) L5. 3241 41