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)

Four hundred and thirty-nine Chinese schizophrenic male patients were investigated for the distribution of haptoglobin types; transferrin and group-specific component subtypes. The allelic frequencies of these three polymorphisms in the patient group were compared with those in healthy controls from published series. An excess of Gc2 over Gc1 (chi 2(1) 4.1; P less than 0.05) as well as a lack of Gc1S (chi 2(1) 15.3; P less than 0.001) was observed in schizophrenia. The relative risks of Gc1F, Gc1S and Gc2 have been estimated as 1.12, 0.76 and 1.15, respectively. It appears from this study that the presence of Gc2 renders individuals susceptible while Gc1S offers protection for schizophrenia. No such association was found for the haptoglobin or transferrin polymorphisms.
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PMID:Serum protein markers in Chinese schizophrenics--haptoglobin types and transferrin and group-specific component subtypes. 230 23

Genetic variants of red-cell acid phosphatase (ACP1), esterase D (ESD), transferrin (TF) and the group-specific component (GC) were investigated in schizophrenic patients with and without a family history of both schizophrenia and other psychiatric disorders. No evident association was found with respect to ACP1, TF and GC systems. A significant difference in the frequency of ESD heterozygotes was found between patients with and without a family history of schizophrenia.
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PMID:Genetic markers in schizophrenia: ACP1, ESD, TF and GC polymorphisms. 236 72

There is some evidence that schizophrenia may be accompanied by alterations in cell-mediated immunity (CMI) and that antipsychotic agents may modulate CMI. The purpose of this study was to investigate the plasma levels of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), sIL-2R, and transferrin-receptor (TfR) in schizophrenia and mania, and the effects of treatment with neuroleptics or mood stabilizers on these variables. The subjects were 14 schizophrenic patients, 10 manic patients and 21 healthy volunteers. The above immune variables were measured in baseline conditions and after treatment with neuroleptics in schizophrenic patients and valproate in manic patients. Plasma concentrations of IL-6, sIL-6R, sIL-2R and TfR were significantly higher in the combined group of psychotic patients than in healthy volunteers. Plasma IL-6 was significantly higher in schizophrenic patients, while plasma sIL-6R and sIL-2R were significantly higher in mania than in normal controls. In schizophrenic patients, plasma levels of IL-6, sIL-6R and TfR were significantly lower after treatment with neuroleptics than before treatment. No significant effects of valproate on the immune-inflammatory markers could be found in the manic patients. It is suggested that activation of CMI may occur in both schizophrenia and mania and that neuroleptics may have immunosuppressive effects through suppression of IL-6 or IL-6R-related mechanisms.
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PMID:Interleukin-2 and interleukin-6 in schizophrenia and mania: effects of neuroleptics and mood stabilizers. 766 81

Using C8 reversed-phase HPLC in conjunction with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, we have fractionated proteins contained in human CSFs obtained from patients with schizophrenic disorders. When these proteins were electrophoretically blotted onto polyvinylidene difluoride membrane for direct N-terminal amino acid sequencing, several CSF proteins were identified; these included albumin, transferrin, apolipoprotein A-I, beta 2-microglobulin, and prealbumin. We have also identified two structurally related human CSF proteins designated cerebrin 28 (M(r) 28,000) and cerebrin 30 (M(r) 30,000) that have an N-terminal amino acid sequence of NH2-APPAQVSVQPNF and NH2-APEAQVSVQPLFXQ, respectively. Comparison of these sequences with existing database at Protein Identification Resource (R 32.0), GenBank (R 72.0), SWISS-PROT (R 22.0), and EMBL (R 31.0) indicated that they are unique proteins. These proteins were subsequently purified by high performance electrophoresis chromatography (HPEC) using an Applied Biosystems 230A HPEC system. A specific polyclonal antibody was prepared and an ELISA was established for cerebrin 30. It was noted that HPEC is a powerful tool to purify microgram quantities of proteins from human, rabbit, and rat CSFs. Using such a system, we have been able to micropurify as many as 10 proteins simultaneously in a single experiment because the elution of proteins occurred strictly according to their molecular weights. More importantly, we routinely obtained a recovery of > 90%. The potential use of this technology for micropurification of proteins was discussed.
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PMID:Micropurification of two human cerebrospinal fluid proteins by high performance electrophoresis chromatography. 833 40

For the early and correct diagnosis of the comorbidity of schizophrenia and alcoholism, a valid laboratory marker would be most helpful in clinical practice. Seventy schizophrenics admitted to a general psychiatric unit of an urban hospital located in a large industrial area in Germany prospectively underwent a detailed addiction history, the Munich Alcoholism Test (MALT) and determinations of serum gamma-glutamyltransferase (gammaGT) and carbohydrate-deficient transferrin (CDT). Cutoff levels for laboratory tests represented the 95th percentile of data obtained from 100 matched healthy controls. Using the MALT, we found evidence of concomitant alcohol consumption in 42.8% of the study patients. The sensitivities of gammaGT and CDT for detecting alcohol abuse (confirmed using DSM III-R criteria) were 70.6 and 58.8%, respectively. Our data suggest that the MALT can be used as a reliable screening test for alcohol use in schizophrenia. In neuroleptic-treated schizophrenics with pathological gammaGT, but low MALT scores, the corresponding CDT may serve as a highly specific marker to verify a concomitant alcohol abuse.
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PMID:Screening for concomitant alcohol abuse in schizophrenia: clinical significance of the Munich Alcoholism Test and laboratory tests. 1039 38

Previous studies have suggested that akathisia is associated with poor acute clinical response to antipsychotics and that low serum iron levels are associated with emergence of akathisia. To examine these relationships during routine clinical treatment, we studied patients with DSM-IV schizophrenia or schizoaffective disorder undergoing hospital treatment for acute psychotic exacerbations with doctor's choice medications. There were 34 subjects observed for at least 2 weeks. They were assessed at baseline and weekly by one rater with the Anchored Brief Psychiatric Rating Scale and by another rater with the Barnes Rating Scale for akathisia, with the two raters blind to each other's ratings. Serum ferritin and transferrin levels were obtained at baseline. Seventeen subjects developed akathisia. Subjects with and without akathisia did not differ in change in thinking disturbance or anxiety-depression scores over 2 weeks, or in serum ferritin or transferrin levels. We conclude that mild akathisia by itself is not strongly associated with initial response to low to moderate doses of antipsychotics in the acute clinical setting. Limitations of the study are discussed.
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PMID:Is akathisia associated with poor clinical response to antipsychotics during acute hospital treatment? 1093 35

As ceruloplasmin and copper abnormalities have been implicated in schizophrenia, we investigated the role of a second copper-containing non-ceruloplasmin protein, the iron oxidase ferroxidase II, in a prospective study of ten inpatients with schizophrenia and a comparison group. Ferroxidase II is a protein known to reciprocally regulate with ceruloplasmin in Wilson's disease, an illness characterized by psychotic symptoms, decreased ceruloplasmin, and increased copper deposition in tissues. Ferroxidase II plays a key role in the maintenance of near-normal iron metabolism in Wilson's disease, but its role in schizophrenia has never been studied. In this study, we assayed ceruloplasmin by two enzymatic assays, a standard clinical laboratory p-phenylenediamine oxidation assay and a second assay based on the rate of the oxidation and incorporation of iron (Fe3+) into transferrin; we assayed ferroxidase II activity using this second iron oxidation assay. We found that ceruloplasmin levels as measured by both enzymatic methods, but not ferroxidase II, were elevated in schizophrenia. The increased ceruloplasmin also correlated with elevated serum copper as assayed by atomic absorption spectrophotometry, which was unsurprising as the majority of copper in blood is bound to ceruloplasmin. It has been proposed that copper, as a component of several enzymes linked to dopamine synthesis, may play a role in schizophrenia by exacerbating or perpetuating dopaminergic dysregulation. Our study suggests that the ceruloplasmin elevation in schizophrenia is specific, and not simply an elevation of plasma copper-containing oxidative enzymes. Increases in ceruloplasmin may result in increased levels of copper, which ultimately proves deleterious in schizophrenia.
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PMID:Plasma copper, iron, ceruloplasmin and ferroxidase activity in schizophrenia. 1684 75

Several recent studies have found changes in the expression of genes functionally related to myelination and oligodendrocyte homeostasis in schizophrenia. These studies utilized microarrays and quantitative PCR (QPCR), methodologies which do not permit direct, unamplified examination of mRNA expression. In addition, these studies generally only examined transcript expression in homogenates of gray matter. In the present study, we examined the expression of myelination-related genes previously implicated in schizophrenia by microarray or QPCR. Using in situ hybridization, we measured transcript expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), myelin-associated glycoprotein (MAG), transferrin (TF), quaking (QKI), gelsolin, myelin oligodendrocyte glycoprotein, v-erb-b2 erythroblastic leukemia viral oncogene homolog 3, erbb2 interacting protein, motility-related protein-1, SRY-box containing gene 10, oligodendrocyte transcription factor 2, peripheral myelin protein 22, and claudin-11 in both gray and white matter of the anterior cingulate cortex (ACC) in subjects with schizophrenia (n=41) and a comparison group (n=34). We found decreased expression of MAG, QKI, TF, and CNP transcripts in white matter. We did not find any differences in expression of these transcripts between medicated (n=31) and unmedicated (n=10) schizophrenics, suggesting that these changes are not secondary to treatment with antipsychotics. Finally, we found significant positive correlations between QKI and MAG or CNP mRNA expression, suggesting that the transcription factor QKI regulates MAG and CNP expression. Our results support the hypothesis that myelination and oligodendrocyte function are impaired in schizophrenia.
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PMID:Expression of transcripts for myelination-related genes in the anterior cingulate cortex in schizophrenia. 1722 13

Several lines of evidence, including diffusion tensor imaging and microarray studies, indicate that abnormalities in myelination play an important role in the pathophysiology of schizophrenia. Of myelin and oligodendrocyte-related genes, a significant decrease in the mRNA levels of transferrin in schizophrenics has been reported by both microarray and quantitative polymerase chain reaction studies. We performed an association analysis of the transferrin gene in a Japanese population of 384 schizophrenic patients and 384 controls. Six single nucleotide polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism and a TaqMan assay. No significant differences in genotype, allele, or haplotype frequencies of the six single nucleotide polymorphisms were observed between schizophrenic patients and controls. The present results suggest that the transferrin gene is not related to the development of schizophrenia in the Japanese population.
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PMID:Association study between the transferrin gene and schizophrenia in the Japanese population. 1749 14

Schizophrenia is likely to be a consequence of serial alterations in a number of genes that, together with environmental factors, will lead to the establishment of the illness. The dorsolateral prefrontal cortex (Brodmann's Area 46) is implicated in schizophrenia and executes high functions such as working memory, differentiation of conflicting thoughts, determination of right and wrong concepts, correct social behavior and personality expression. We performed a comparative proteome analysis using two-dimensional gel electrophoresis of pools from 9 schizophrenia and 7 healthy control patients' dorsolateral prefrontal cortex aiming to identify, by mass spectrometry, alterations in protein expression that could be related to the disease. In schizophrenia-derived samples, our analysis revealed 10 downregulated and 14 upregulated proteins. These included alterations previously implicated in schizophrenia, such as oligodendrocyte-related proteins (myelin basic protein and transferrin), as well as malate dehydrogenase, aconitase, ATP synthase subunits and cytoskeleton-related proteins. Also, six new putative disease markers were identified, including energy metabolism, cytoskeleton and cell signaling proteins. Our data not only reinforces the involvement of proteins previously implicated in schizophrenia, but also suggests new markers, providing further information to foster the comprehension of this important disease.
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PMID:Proteomic analysis of dorsolateral prefrontal cortex indicates the involvement of cytoskeleton, oligodendrocyte, energy metabolism and new potential markers in schizophrenia. 1911 Feb 65


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