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 presentation deals with catalase activity in the whole blood and in the leukocytes of patients with nuclear schizophrenia. The catalase activity in the whole blood was higher than in normals. During insulin shock the enzyme activity both in the blood and leukocytes was significantly higher. A low catalase activity in the blood leukocytes in patients with nuclear schizophrenia may be conditioned by a drop in the aerobe respiration and oxidative phosphorilyzing of leukocyte mitochondria.
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PMID:[Catalase in the blood and leukocytes of patients with nuclear schizophrenia]. 93 50

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

Previous studies found peripheral activities of antioxidant enzymes to be abnormal in schizophrenic patients. It is not understood whether this is integral to the disease process or a result of long-term treatment with neuroleptics. Red blood cell activities of three antioxidant enzymes--superoxide dismutase, glutathione peroxidase, and catalase--were therefore examined in 14 drug-naive, first episode patients with a diagnosis of schizophrenia or schizophreniform disorder and 10 normal subjects. The patients had an average duration of psychosis of 4.46 days (SD 2.5). Superoxide dismutase activity was significantly lower in patients than in normal controls, with no difference between the groups in activities of the other two enzymes. Lower superoxide dismutase activity was associated with deterioration of school functioning from childhood to early adolescence and a history of poorer school functioning during early adolescence. These findings indicate a compromised antioxidant defense at the onset of psychosis, and suggest that oxidative injury might contribute to adverse developmental events in the pathogenic cascade of schizophrenia.
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PMID:Impaired antioxidant defense at the onset of psychosis. 914 92

Thirty-eight patients diagnosed as having continuous schizophrenia progrediens, 35 patients with shift-like schizophrenia and six patients with hypertoxic (feverish) schizophrenia were studied. The examinees displayed a marked increase in the blood content of lipid peroxidation products, such as malonic dialdehyde and conjugated dienes, together with an enhancement of the degree of erytrocytolysis, which events are particularly noticeable in hypertoxic- and continuous schizophrenia. Blood catalase activity gets higher, that of superoxide dismutase is on the decrease, which facts suggest to us some faults in the system of antioxidant defence.
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PMID:[The level of lipid peroxidation and the function of the antioxidant system in different forms of schizophrenia]. 979 17

This paper reviews what is currently known about the redox state of the glutamate synapse and its possible role in modulating synaptic plasticity and thus learning and neurocomputation. The hypothesis is presented that the growth or pruning of the synaptic spine is controlled in part by the balance in the synapse between neurodestructive pro-oxidants (e.g., nitric acid radical and hydrogen peroxide) and neuroprotective antioxidants (e.g., ascorbate and carnosine). In addition, there may be a role for catecholamines, in particular dopamine, related to its role in reinforcement signalling. Activation of the dopamine D2 receptor induces the synthesis of an antioxidant enzyme, possibly catalase. Dopamine may also affect the redox balance in the glutamate synapse directly by diffusion from the adjacent dopaminergic bouton-en-passage. Catecholamines are powerful antioxidants, scavengers of free radicals and iron chelators. Catecholamine-iron complexes are potent dismuters of superoxide ions. Additional agents participating in spine pruning may be neurotoxic catecholamine o-quinones present in the brain. This system may be at fault in schizophrenia and Parkinson's disease. Experiments to test the hypothesis are suggested.
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PMID:Redox mechanisms at the glutamate synapse and their significance: a review. 1032 73

In order to examine antioxidant status and lipid peroxidation in schizophrenia patients, activities of three free radical scavenging enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)), and the level of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation have been studied in red blood cells. Schizophrenic patients were divided into three groups (disorganized (n = 21), paranoid (n = 26) and residual types (n = 18)) to determine differences between subgroups. SOD, CAT and GSH-Px activities in the control group were found to be 1461.0 +/- 248.6 U g(-1) Hb, 148.2 +/- 59.3 k g(-1) Hb and 25.87 +/- 4.25 U g(-1) Hb, respectively. We found no significant differences in SOD activities between study and control groups. There was a significant increase in SOD activity in the residual group compared to the paranoid group (P < 0.005). CAT activity was found to be increased in disorganized (148%), paranoid (147%), and residual (165%) groups compared to the control group. GSH-Px activity was markedly increased in the study groups except the paranoid group. Statistically significant (3-4 fold) increases in TBARS levels of red blood cells were found in all the study groups. It is proposed that antioxidant status may be changed in schizophrenia and thus may induce lipid peroxidation. Therefore, oxidative stress may have a pathophysiological role in all the subtypes of schizophrenia.
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PMID:Evidence that the activities of erythrocyte free radical scavenging enzymes and the products of lipid peroxidation are increased in different forms of schizophrenia. 1124 87

Two substances which are products of the isoprenoid pathway, can participate in lipid peroxidation. One is digoxin, which by inhibiting membrane Na(+)-K+ ATPase, causes increase in intracellular Ca2+ and depletion of intracellular Mg2+, both effects contributing to increase in lipid peroxidation. Ubiquinone, another products of the pathway is a powerful membrane antioxidant and its deficiency can also result in defective electron transport and generation of reactive oxygen species. In view of this and also in the light of some preliminary reports on alteration in lipid peroxidation in neuropsychiatric disorders, a study was undertaken on the following aspects in some of these disorders (primary generalised epilepsy, schizophrenia, multiple sclerosis, Parkinson's disease and CNS glioma)--1) concentration of digoxin, ubiquinone, activity of HMG CoA reductase and RBC membrane Na(+)-K+ ATPase 2) activity of enzymes involved in free radical scavenging 3) parameters of lipid peroxidation and 4) antioxidant status. The result obtained indicates an increase in the concentration of digoxin and activity of HMG CoA reductase, decrease in ubiquinone levels and in the activity of membrane Na(+)-K+ ATPase. There is increased lipid peroxidation as evidenced from the increase in the concentration of MDA, conjugated dienes, hydroperoxides and NO with decreased antioxidant protection as indicated by decrease in ubiquinone, vit E and reduced glutathione in schizophrenia, Parkinson's disease and CNS glioma. The activity of enzymes involved in free radical scavenging like SOD, catalase, glutathione peroxidase and glutathione reductase is decreased in the above diseases. However, there is no evidence of any increase in lipid peroxidation in epilepsy or MS. The role of increased operation of the isoprenoid pathway as evidenced by alteration in the concentration of digoxin and ubiquinone in the generation of free radicals and protection against them in these disorders is discussed.
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PMID:Isoprenoid pathway and free radical generation and damage in neuropsychiatric disorders. 1127 6


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