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)

The authors evaluated 108 patients with schizophrenia, 50 patients with affective disorder, and 74 age- and sex-matched control subjects by CAT scan for evidence of global cerebellar atrophy. No difference was found between control subjects and schizophrenic patients or between control subjects and patients with affective disorder. This study does not confirm previous reports linking cerebellar atrophy to schizophrenia.
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PMID:Cerebellar atrophy in schizophrenia and affective disorder. 356 15

Data are presented on 24 patients with epilepsy and psychosis whose clinical presentation was rated using the Present State Examination (PSE). Seventeen had complex partial seizures and a diagnosis of temporal lobe epilepsy, seven had generalised epilepsy. An association between a CATEGO category of nuclear schizophrenia (NS) and a lesion of the left side was noted. No clear link between depressive symptoms and a right-sided focus was discovered. Affective disorders were noted in both groups of epileptic patients, although paranoid psychoses were commoner in the temporal lobe group. There was also a tendency for the latter to have more delusions of persecution, ideas of reference, and special features of depression. The group rated as NS appear less likely to show evidence of intellectual deterioration than the other psychotic patients; in addition, the interval between the onset of their epilepsy and the onset of their psychosis is shorter. Radiological assessment by CAT reveals few differences between groups, but the psychotic samples do show higher than expected values on a number of variables, in particular the bilateral septum-caudate distance and the size of the third and fourth ventricle.
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PMID:Epileptic psychosis: an evaluation of PSE profiles. 397 33

CAT scan studies linking schizophrenia to structural pathology of the brain are critically reviewed. CAT findings implicate an irreversible, static process, probably occurring early in development and resulting in a reduction of brain mass. The specificity of the process cannot be assessed from CAT images. Clinical correlations suggest that greater structural change is associated with more clinical neurological signs, suggestive of a pathological continuum rather than a sub-group concept. The CAT images are consistent with recent postmortem evidence of limbic-diencephalic pathology in schizophrenia. A structural deficit hypothesis is proposed.
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PMID:Computed tomography (CT) findings in schizophrenia: speculation on the meaning of it all. 609 37

There is increasing evidence that free radical-mediated CNS neuronal dysfunction is involved in the pathophysiology of schizophrenia. Free radicals (oxyradicals, such as superoxide, hydroxyl ions, and nitric oxide) cause cell injury when they are generated in excess or the antioxidant defense is impaired. Both of these processes seem to be affected in schizophrenia. Evidence of excessive oxyradical generation is premised on the assumption that there is increased catecholamine turnover, though there is little direct evidence to support such a view, which is further accentuated by neuroleptic treatment. However, antioxidant enzymes (superoxide dismutase, SOD; glutathione peroxidase, GSHPx; and catalase, CAT) which are constitutively expressed in all tissues, are found to be altered in erythrocytes of schizophrenic patients. Also, possible oxyradical-mediated injury to CNS is suggested by increased lipid peroxidation products in cerebrospinal fluid and plasma, and reduced membrane polyunsaturated fatty acids (PUFAs) in the brain and RBC plasma membranes. The brain is more vulnerable to oxyradical-mediated injury,because its membranes are preferentially enriched in oxyradical sensitive PUFAs, and damaged adult neurons cannot be replaced. In addition to their pathological role, oxyradicals have critical physiological functions in neuronal development, differentiation, and signal transduction, all of which may be altered in some cases of schizophrenia. It may be possible to define cellular injury processes, investigate underlying dynamic regulatory molecular processes, and find ways to prevent these injury processes using peripheral cell models, e.g., red blood cells, lymphocytes and cultured skin fibroblasts. Information on the clinical implications of these processes are valuable for developing new and innovative therapeutic strategies for schizophrenia.
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PMID:Free radical pathology and antioxidant defense in schizophrenia: a review. 914 91

The primary goal of this study was to investigate transfer of training (generalization) in patients with schizophrenia. We randomly assigned 33 schizophrenia subjects to one of three conditions: training on the Wisconsin Card Sort Test (WCST-T), training on the Halstead Category Test (CAT-T), or no training (No-T). The WCST and CAT were administered to all subjects at baseline. Subjects in the WCST-T and CAT-T groups then received training on the respective test, while the No-T group received additional untrained trials. All participants were subsequently retested on the WCST and CAT, and completed a brief neuropsychological battery. As hypothesized, the WCST-T and CAT-T groups exhibited large improvements on the trained test and moderate improvement on the untrained test, while the No-T group failed to show improvement on either test. These results suggest that the training paradigm did produce generalization, and that the changes were not due to practice effects. The extent of generalization across both training groups was strongly associated with neuropsychological test performance (Spearman's rho=0.56, P<0.05). The implications of these findings for rehabilitation programs were discussed, and recommendations were made for future research.
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PMID:Generalization of training effects in schizophrenia. 1129 78

Oxidative stress-mediated cell damage has been considered in the pathophysiology of schizophrenia. Abnormal findings have often been considered related to differences in ethnicity, life style, dietary patterns and medications, all of which influence indices of oxidative stress and oxidative cell damage. To minimize these confounds, schizophrenic patients were compared with age-matched control subjects with the same ethnic background and similar lifestyle, as well as with bipolar mood disorder (BMD) patients. Levels of antioxidant defense enzymes (i.e. superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GPx) were lower in schizophrenic patients than in controls, indicating conditions for increased oxidative stress. The contents of plasma thiobarbituric acid reactive substances (TBARS) were only marginally higher in schizophrenic patients, who had normal levels of arachidonic acid (AA), a major source of TBARS, indicating no significant oxidative membrane lipid peroxidation. Levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), however, were significantly lower in schizophrenic patients. When the same indices in BMD patients were compared with findings in matched controls, levels of only SOD and CAT were lower in the patients, whereas GPx was not. Again, as in schizophrenia, the contents of TBARS were marginally higher in BMD patients with no change in levels of AA. Levels of alpha-linolenic acid and EPA were significantly lower and levels of DHA were slightly lower in BMD patients. These data indicate that certain biochemical characteristics may be common to a spectrum of psychiatric disorders, and suggest supplementation of antioxidants and essential fatty acids might affect clinical outcome.
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PMID:Decreased antioxidant enzymes and membrane essential polyunsaturated fatty acids in schizophrenic and bipolar mood disorder patients. 1465 46

We identified CAT 53 by cDNA hybridization selection as an expressed sequence tag (EST), located in the vicinity of HLA-C and designated as CAT (for HLA-C associated transcript) 53. CAT 53 encodes a protein described by others and commonly known as phosphatase 1 nuclear targeting subunit (PNUTS). PNUTS is a potent inhibitor of nuclear serine/threonine protein phosphatase 1 (PP1). We present the genomic organization of CAT 53, localize specific sites of mRNA transcription in thin sections of mouse brain by in-situ hybridization, and perform a structural analysis of the peptide domains. We also characterize the protein expression pattern for PNUTS by Western blotting and immunohistochemistry with PNUTS antibody in Alzheimer's disease (AD) brains and age-matched control brains. In-situ hybridization and immunohistochemistry analysis of human and mouse brain show high CAT 53 expression in the olfactory cortex, piriform cortex, and hippocampus. Very high expression of CAT 53 was found mainly in the hippocampus, frontal, and entorhinal cortex of control brains and in the neurofibrillary tangles of AD brain. In the hippocampus, CAT 53 is expressed in CA1 and CA3 cell layers and in the dentate gyrus. The hippocampus is known to play a fundamental role in learning and episodic memories and has been implicated in a number of neurological and psychiatric disorders, including AD, epilepsy, and schizophrenia. Our findings suggest that PNUTS, encoded by CAT 53 on 6p21.3, may have a role in the progression of AD.
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PMID:CAT 53: a protein phosphatase 1 nuclear targeting subunit encoded in the MHC Class I region strongly expressed in regions of the brain involved in memory, learning, and Alzheimer's disease. 1589 2

We examined the efficacy of 2 treatments using environmental supports (e.g. signs, alarms, pill containers, checklists) to improve functional outcomes in individuals with schizophrenia. 120 participants were randomized into one of 3 treatment groups 1) Cognitive Adaptation Training (CAT; supports customized to individual cognitive impairments and behaviors and maintained on weekly home visits 2) Generic Environmental Supports (GES; a generic set of supports given to patients at a routine clinic visit and replaced on a monthly basis) and 3) treatment as usual (TAU). Functional outcomes, positive symptoms and motivation were assessed at baseline, 3, 6, 9, 18 and 24 months. After 9 months of intensive treatment with CAT, visits were decreased from weekly to monthly to examine whether treatment gains could be maintained. Results of a mixed effects regression model with repeated measures indicated a significant main effect of group (CAT>GES>TAU) with non-significant time and group by time interactions. Post-hoc analyses indicated that while individuals in CAT remained significantly better than those in TAU when treatment frequency was reduced, gains in CAT decreased to the level of those seen in GES. While group differences for positive symptoms were not significant, motivation improved in CAT and GES relative to TAU. The highest intensity treatment produced the best outcomes with respect to functioning. However, some improvements were seen with a relatively inexpensive, clinic-based treatment using a package of generic environmental supports.
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PMID:Comparing the efficacy of interventions that use environmental supports to improve outcomes in patients with schizophrenia. 1837 42

Cognitive remediation is a type of treatment added recently to the range of tools available to therapists. It includes a number of miscellaneous methods that aim to correct some of the cognitive impairments observed in schizophrenia. These cover the fields of target attention, memory and executive deficits, as well as impaired social cognition. Cognitive remediation acts as a complement to medication and psychological therapies, which constitute the core methods of treatment for schizophrenia. The present paper reviews the state of the art in cognitive remediation. The principle underlying this innovative therapeutic approach is the enhancement of the cognitive resources of patients with schizophrenia in order to improve their cognitive functions, social skills and in some cases alleviate some of the symptoms of the disease. Several programs developed within the past two decades (e.g., IPT, CRT, NEAR, CET, NET, CRT and CAT) are becoming more widely used. Their efficacy on neurocognition and on functional outcome has been demonstrated, with inconstant continuation of benefit after completion of treatment. The sustainability of the cognitive and functional improvements following completion of these programs has to be further studied. Other programs aimed at acting upon altered social cognition (one of the critical facets of schizophrenia) are still in the experimental stages, but the results obtained so far are encouraging. A preliminary study has also demonstrated the effectiveness of board games in improving cognitive functioning, which seems to be a highly promising therapeutic avenue owing to its ease of use.
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PMID:Cognitive remediation: a promising tool for the treatment of schizophrenia. 1859 Apr 74

Schizophrenia is a complex neuropsychiatric disorder in which symptoms can be classified as either positive, such as delusions and hallucinations, or negative, such as blunted affect and social withdrawal. However, the mechanisms underlying this disease are poorly understood. There is evidence that reactive oxygen species (ROS) play an important role in the pathogenesis of many diseases, particularly those which are neurological and psychiatric in nature. Ketamine has been used to induce a schizophrenia-like condition as an animal model in which to study this condition. In the present study we tested the effects of sub-anesthetic doses of ketamine on various parameters of oxidative stress in the brain of rats. Our results indicate that lipid peroxidation and tissue protein oxidation were affected by varying sub-anesthetic doses of ketamine in multiple cerebral structures. Additionally, the activity of the antioxidant enzymes CAT and SOD was measured and was also found to be altered in most of the structures tested. In conclusion, we observe an increase in oxidative damage marked by an increase in lipid peroxidation, oxidative protein damage and a decrease in enzymatic defenses, in an animal model of schizophrenia. Given that oxidative stress could be related to schizophrenia, these findings may explain, at least in part, the mechanisms underlying in this disease.
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PMID:Different sub-anesthetic doses of ketamine increase oxidative stress in the brain of rats. 1945 99


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