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)

A 39-year-old female with several past psychiatric hospitalization for schizophrenia was admitted to our hospital because of severe pain and swelling of her legs. A few days before onset, she had often sat down upon her heels in water closet, agitated and talking to herself for many hours. Two days before the admission, she had suffered from severe pain and swelling of her bilateral calf-muscles, and her urine became brownish. On admission, neurological findings revealed delirious state, moderate rigidity of limbs, hyporeflexia of legs, marked swelling and severe spontaneous pain in bilateral legs. She was afebrile with body temperature of 36.4 degrees C. Laboratory data showed marked increase of levels of serum CK to 163,000 U/1, myoglobin to 9,860 ng/ml and aldolase to 42.8 IU/1, and the diagnosis of rhabdomyolysis was made. Although she fell into acute renal failure, the renal function recovered after repeated hemodialysis. Several days after admission, swelling and pain of calf-muscles began to improve, and serum CK, myoglobin and aldolase decreased rapidly. One month later, she was able to walk on her own legs. In the literature, rhabdomyolysis associated with immobile posture caused by schizophrenia is extremely rare, and this is the first case reported in Japan. The relationship between rhabdomyolysis and schizophrenia was discussed.
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PMID:[A case of rhabdomyolysis following long time immobile posture caused by schizophrenia]. 259 45

The dystrophin-associated protein complex (DPC), comprising sarcoglycans, dystroglycans, dystrobrevins, and syntrophins, is a component of synapses both in muscle and brain. Dysbindin is a novel component of the DPC, which binds to beta-dystrobrevin and may serve as an adaptor protein that links the DPC to an intracellular signaling cascade. Disruption of the DPC results in muscular dystrophy, and mutations in the human ortholog of dysbindin have been implicated in the pathogenesis of schizophrenia. In both cases, patients also present with neurological symptoms reminiscent of cerebellar problems. In the mouse cerebellum, dysbindin immunoreactivity is expressed at high levels in a subset of mossy fiber synaptic glomeruli in the granular layer. Lower levels of dysbindin immunoreactivity are also detected in Purkinje cell dendrites. In the cerebellar vermis, dysbindin-immunoreactive glomeruli are restricted to an array of parasagittal stripes that bears a consistent relationship to Purkinje cell parasagittal band boundaries as defined by the expression of the respiratory isoenzyme zebrin II/aldolase c. In a mouse model of Duchenne muscular dystrophy, the mdx mutant, in which dystrophin is not expressed, there is a dramatic increase in the number of dysbindin-immunoreactive glomeruli in the posterior cerebellar vermis. Moreover, the topography of the terminal fields is disrupted, replacing the stripes by a homogeneous distribution. Abnormal synaptic organization in the cerebellum may contribute to the neurological problems associated with muscular dystrophy and schizophrenia.
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PMID:Abnormal dysbindin expression in cerebellar mossy fiber synapses in the mdx mouse model of Duchenne muscular dystrophy. 1287 99

Two-dimensional gel-electrophoresis in combination with mass spectrometry is a powerful approach to compare protein expression in brain tissues. Using this proteomic approach, and based on the hypothesis that schizophrenia involves hypoglutamergic brain function, alterations in protein levels in the thalamus of rats treated with the N-methyl-D-aspartate (NMDA) receptor antagonist [+]-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]-cycloheptene-5,10-iminehydrogenmaleate (MK-801), as compared to saline-treated animals, were assessed in an unbiased fashion. The rats were divided into two groups; group 1 (short-term treated) and group 2 (long-term treated). In group 1, the levels of seven proteins were increased and four proteins reduced. In group 2, the levels of six proteins were reduced. Several of the altered proteins (heat shock proteins 60 and 72, albumin, dihydropyrimidinase related protein-2, aldolase c, and malate dehydrogenase) have previously been connected to schizophrenia. Alterations of other proteins (dihydrolipoamide acetyltransferase component of pyruvate dehydrogenase complex E2, guanine deaminase, alpha-enolase, aconitase, ATP-synthase and alpha-internexin), have not, to the best of our knowledge, earlier been implicated in schizophrenia pathology. Our results show the high potential of using proteomic methods for the validation of animal models of schizophrenia and to identify new proteins involved in the pathophysiological mechanisms of schizophrenia.
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PMID:Comparative proteome analysis of thalamus in MK-801-treated rats. 1499 2