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 newly developed assay for monoamine oxidase (MAO) activity in blood platelets (serotonin used as substrate) was applied for the measurement of the enzyme activity in 76 schizophrenic patients. No significant reduction was found in the blood platelet MAO activity in a group of 33 untreated schizophrenic patients, as compared to that in the normal controls. Male patients revealed to have lower enzyme activity than females in the schizophrenic group, as we described previously in the normal subjects. Treatment with phenothiazines caused significant reduction of blood platelet MAO activity, while platelet serotonin content and platelet count appeared to be not affected by the drug treatment. The authors suggest that blood platelet MAO activity may be related to hormonal factors but not to psychiatric diagnosis of schizophrenia or constitution liable to schizophrenic illnesses.
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PMID:Reduction of blood platelet monoamine oxidase activity in schizophrenic patients on phenothiazines. 0 24

This review surveys the therapeutic efficacy of tricyclic antidepressants and monoamine oxidase inhibitors in schizophrenic patients. In general, the use of these drugs alone was found not to be warranted in schizophrenia, except perhaps in the so-called pseudoneurotic subgroup. In most cases, combinations of antidepressants and phenothiazines were not more beneficial than phenothiazines alone. In particular, the conditions of agitated patients and patients with histories of social deviance dating back to childhood were often made worse by the addition of an antidepressant. However, when the patients who demonstrated symptoms of clinical depression other than anergia were isolated from several of these studies, it was found that they constituted a subgroup that was often benefited by use of these combinations. Favorable and unfavorable clinical response patterns are discussed, and recommendations for future research are outlined.
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PMID:Use of antidepressant drugs in schizophrenia. 3 Apr 29

A study was made of platelet monoamine oxidase (MAO) activity in non-medicated, newly-admitted schizophrenics and institutionalized chronic schizophrenics both on and off medication. These patients were compared to two control groups: normal subjects and brain-damaged institutionalized patients. No relationship was found between platelet MAO activity and the severity or duration of illness, duration of psychotropic medication, presence of auditory hallucinations or institutionalization. Mean platelet MAO activity did not differ significantly between the schizophrenic subgroups and control groups. Thirty-one patients studied before and after treatment with phenothiazines showed no significant change in platelet MAO activity. The findings did not indicate a relationship between schizophrenia, its treatment or outcome and platelet MAO activity.
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PMID:Platelet monoamine oxidase activity in schizophrenia. Relationship to disease, treatment, institutionalization and outcome. 3 92

Dopamine and its metabolites homovanillic acid and dihydroxyphenylacetic acid, noradrenaline, serotonin and its metabolite 5-hydroxyindoleacetic acid, and tryptophan and its metabolite kynurenine have been assayed in 9 schizophrenic and 10 control brains, together with the monoamine-related enzymes tyrosine hydroxylase monoamine oxidase, dopamine-beta-hydroxylase, and catechol-o-methyl-transferase. In schizophrenic brains dopamine, noradrenaline and serotonin were significantly increased in some areas of corpus striatum, but there were no significant changes in enzyme activity or monoamine metabolite concentrations in any of the brain areas examined. The findings are not consistent with theories that serotonin or noradrenaline stores are grossly depleted or noradrenaline neurones have degenerated, or that monoamine oxidase activity is abnormal, in schizophrenia, and provide no direct support for the hypothesis that dopamine neurones are overactive.
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PMID:Monoamine mechanisms in chronic schizophrenia: post-mortem neurochemical findings. 4 9

Platelet monoamine oxidase (MAO) is under genetic control. A lower MAO activity in chronic schizophrenia has repeatedly been reported, and it has been suggested that reduced activity of this enzyme reflects an increased vulnerability to schizophrenia. To test this hypothesis platelet MAO was determined in 65 first-degree relatives of 22 schizophrenic index patients and in matched healthy controls. No difference in mean activity between the two samples could be detected, suggesting that reduced MAO activity in schizophrenia is more likely to be a phenomenon secondary to the disease. A significant parent-offspring correlation of MAO activities was obtained.
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PMID:Platelet monoamine oxidase activity in first-degree relatives of schizophrenic patients. 11 98

A study of the activity of leukocyte enzymes in the blood of patients with nuclear forms of schizophrenia (52 cases) and in patients with circular schizophrenia (22 cases) depicted the following conditions. In the group of malignant schizophrenia, irrespective of the stage of the disease and in the group of circular forms there was a definite drop in the activity of cytochromoxidase, succinatedehydrogenase and MAO, while as the activity of the ATP-ase and peroxidase was increased. Supplementary animal experiments in vitro and in vivo made it possible to assume that these changes are due to the so-called serum factor.
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PMID:[The effect of schizophrenic patients serum on the activity of several leukocyte enzymes]. 17 27

Plasma levels of flupenthixol were estimated by three methods in 30 patients with acute schizophrenia and 29 patients with chronic schizophrenia. These levels were related to clinical response, anterior pituitary hormone secretion, platelet monoamine oxidase activity, the effects of the concurrent administration of anticholinergic drugs, and body weight. No clearcut relationships between plasma flupenthixol levels and any of these variables were demonstrated. The practical clinical value of the estimation of plasma flupenthixol is limited at the present time.
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PMID:Blood levels of flupenthixol in patients with acute and chronic schizophrenia. 26 91

Platelet monoamine oxidase (MAO) was kinetically evaluated in chronic schizophrenics and matched controls, using substrates of major physiologic importance and substrates of particular interest in the study of schizophrenia, such as serotonin (5-ht), N,N-dimethyltryptamine (DMT), 5-methoxytryptamine (5-MT), and dopamine (DA). Substrates were measured at six concentrations; values for maximal velocity (Vmax) and Michaelis constant (Km) were obtained by using Lineweaver-Burk plots. The Vmax was decreased for all substrates in chronic schizophrenia and the Km was decreased for DA, 5-HT, and DMT, but remained unchanged for 5-MT. The value of Km/Vmax was similar for schizophrencis and normal persons when DA, 5-HT, and DMT were used as substrates, which may indicate that "uncompetitive" inhibition is responsible for the observed decrease in activity among chronic schizophrenics. The finding of a decreased Vmax but unchanged Km with 5-MT would be consistent with noncompetitive inhibition.
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PMID:Decreased platelet monoamine oxidase activity in chronic schizophrenia, shown with novel substrates. 28 95

The transmethylation hypothesis of schizophrenia was reviewed with considerations that large doses of methionine when combined with a monoamine oxidase inhibitor lead to exacerbation of psychotic symptoms in a significant percentage of chronic schizophrenic patients. It was noted that nicotinic acid in the dosage of 3,000 mg/day can neither prevent nor counteract the psychopathology thus induced.
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PMID:Transmethylation hypothesis of schizophrenia: methionine and nicotinic acid. 33 34

The authors review studies of platelet and white cell monoamine oxidase (MAO) activity in schizophrenic patients. The data on acute schizophrenic patients remain inconclusive. Review of 26 reports of chronic schizophrenic patients leaves little doubt, however, that there is a subgroup in which the enzyme activity is decreased. Despite the strong association of decreased MAO activity and chronic schizophrenia, the etiological relationship of low platelet MAO activity to schizophrenia has not been demonstrated. More complete diagnostic descriptions will shed light on precisely which patients have lowered MAO activity. Further metabolic investigations with such patients are needed to determine the physiological significance of this phenomenon.
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PMID:Platelet monoamine oxidase activity in schizophrenia: a review of the data. 37 19


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