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)

As part of a prospective, psychosocial, and biochemical study of infectious mononucleosis, platelet monoamine oxidase (MAO) activity has been evaluated as a host factor. It was found that platelet MAO activity may be a possible predisposing host factor but not a precipitating factor. The results on infectious mononucleosis, a viral disease which involves the host's cell-mediated immune system, are compared with an evaluation of platelet MAO activity in dengue, a viral disorder involving the host's humoral immune system. The platelet MAO activity in these disorders has been compared to that in schizophrenia, a disease for which low platelet MAO activity has been postulated, from retrospective and twin studies, to be a risk factor. One hypothesis suggests that low platelet MAO activity predisposes to development of schizophrenia, but also increases cell-mediated immune system responses.
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PMID:Studies of platelet monoamine oxidase activity in Epstein-Barr and dengue virus infections. 624 72

The authors compare schizophrenia with several other diseases and discuss how a few simple models that have already been successfully applied in other cases could be used in the genetic analysis of schizophrenia and MAO activity. Among the diseases discussed are Huntington's disease, xanthomatosis, and diabetes. The authors recommend undertaking multivariate studies of monoamine oxidase, dopamine beta-hydroxylase, and other traits associated with schizophrenia in single, large pedigrees ascertained through schizophrenic probands.
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PMID:Types of disease and models for their genetic analysis. 644 88

The most readily available source of monoamine oxidase in man is the platelet, although only the B form of the enzyme is represented in this site. Platelet activity is higher in women than in men. The enzyme activity is generally stable and is partly under genetic control. There is some evidence that individuals with low activity have a higher psychiatric morbidity than those with high activity. Despite some negative studies, the consensus of publication dealing with schizophrenia, migraine, and alcoholism find that mean platelet monoamine oxidase activity in the patient group is lower than in the controls. Values are raised in unipolar depression. Technical differences, or patient or control group heterogeneity, might well account for the absence of unanimity in the literature. A considerable degree of overlap between patient and control values, whatever the clinical diagnosis, appears to be the standard finding. Apart from these neuropsychiatric disturbances, platelet monoamine oxidase activity is raised in megaloblastic anaemia and reduced in iron deficiency anaemia. Although altered enzyme activity values may be linked to abnormal platelet populations in some of the haematological disorders discussed, in general the causes of abnormal platelet monoamine oxidase activity are unknown.
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PMID:Human platelet monoamine oxidase activity in health and disease: a review. 645 37

Platelet monoamine oxidase activity (MAO) was determined in 39 unmedicated chronic schizophrenic patients and 88 normal control subjects. Platelet MAO activity did not distinguish paranoid from nonparanoid patients or patients who met Taylor and Abrams criteria for narrowly defined schizophrenia from other schizophrenics. Enzyme activity was not related to either prognostic scores or age at onset of illness. MAO activity was decreased in patients compared to controls, and was lower in males than in females. Our findings indicate that clinical phenomenology, as defined in the present study, is of limited use in identifying biological subtypes of schizophrenia with deviant platelet MAO activity.
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PMID:Platelet monoamine oxidase and clinical phenomenology of schizophrenia. 658 13

Platelet monoamine oxidase (MAO) activity was compared in four age and sex-matched groups: monozygotic (MZ) twins discordant for schizophrenia, normal MZ twins, normal dizygotic (DZ) twins and unrelated individuals. Among the twin groups, schizophrenic and normal there was a remarkably consistent degree of genetic control amounting to 70-80 per cent of the variation in activity. The mean platelet MAO activity of the schizophrenic twins was significantly lower than that of controls, but not than that of their psychiatrically well, neuroleptic-free cotwins; indeed the correlation for the MZ twins discordant for schizophrenia was almost exactly the same as that for the normal MZs. Thus, lower platelet MAO activity in schizophrenia, where it is found, is genetically modulated and not the result of the illness or its treatment.
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PMID:Genetics of platelet MAO activity in discordant schizophrenic and normal twins. 668 83

Urinary phenylacetic acid (PAA) excretion was found to be decreased in a group of chronic schizophrenic patients, particularly in a nonparanoid subtype. No significant change in PAA excretion was observed in a group of 21 unipolar depressed patients. Urinary PAA was studied following the administration of phenylethylamine, monoamine oxidase inhibitors, a dopa decarboxylase inhibitor, a low phenylalanine diet, and phenylalanine loads in several groups of psychiatric patients and normal volunteers. While Phenylethylamine ingestion increased urine PAA, inhibition of both phenylethylamine metabolism and synthesis failed to alter urine PAA. These studies suggest that urine PAA is primarily derived from phenylalanine transamination or pathways not involving monoamine oxidase or both. The observed decrease in PAA excretion in some schizophrenic patients may reflect an alteration in this pathway. The high phenylethylamine excretion previously reported in some chronic schizophrenic patients is not directly related to the observed low PAA excretion. Therefore measurement of urine PAA is not expected to be useful in assessing any phenylethylamine abnormalities in psychiatric disorders. The possible contribution of reduced phenylalanine transamination and its subsequent increased availability for the possible synthesis of phenylethylamine in schizophrenia is discussed.
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PMID:Phenylacetic acid excretion in schizophrenia and depression: the origins of PAA in man. 671 36

Platelet monoamine oxidase (MAO) activity, determined in 102 patients with chronic schizophrenia, 223 first-degree relatives, and 88 normal control subjects, was shown to be a heritable and stable trait and was significantly lower in patients than in normal control subjects. Within families, MAO activity distinguished ill from well relatives. However, the considerable overlap in enzyme activity between affected and unaffected individuals limits the usefulness of low MAO activity as a major risk factor in schizophrenia.
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PMID:Platelet monoamine oxidase activity and genetic vulnerability to schizophrenia. 673 31

Platelet monoamine oxidase (MAO) activity was determined in a large population of drug-free and haloperidol-treated schizophrenic patients and healthy controls and, in a second study, in a sample of schizophrenics after a wash-out period and at different times during treatment with haloperidol. Enzyme activity was significantly decreased in both acute and chronic haloperidol-treated schizophrenics, but not in drug-free schizophrenics, compared with normal controls. No significant difference was observed between drug-free schizophrenics with a family history of the illness and those without such history, and between healthy relatives of schizophrenic patients and normal controls without a family history of schizophrenia. MAO activity was significantly reduced after 14 and 21 days of haloperidol treatment, and such reduction did not correlate with response to treatment. These data strongly support the idea that neuroleptic intake may, at least in part, explain low MAO values repeatedly reported in schizophrenics.
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PMID:Platelet monoamine oxidase activity in schizophrenia: relationship to family history of the illness and neuroleptic treatment. 674 11

This is a review of the present state of knowledge in the area of biological markers that may delineate subpopulations of patients with major psychotic illness. Postmortem studies have revealed that schizophrenia is associated with an excess of dopamine (DA) receptors in the limbic system. A more clinically useful adaptation of this approach has been a study of DA D2 receptors in lymphocytes. Studies of monoamine oxidase, dopamine-beta-hydroxylase, and dimethyltryptamine have not fulfilled their early promise nor have the peptides provided useful information as to possible biological markers. Recent studies of the one-carbon cycle enzymes, methionine adenosyltransferase and serine hydroxymethyltransferase, suggest that underactivity of these, particularly the former, may be a reliable clinical marker for a subgroup of schizophrenics. The computerized axial tomography (CAT) scan abnormalities of schizophrenia establish useful indices of abnormal cerebral anatomy such as cortical atrophy with enlarged ventricles, cortical asymmetries, and atrophy of the cerebellar vermis. Positron emission tomography studies with 18F 2-deoxyglucose (2DG) have shown that many schizophrenics have a higher 2DG uptake in the occipital and temporal rather than the frontal cortex, thus reversing the normal patterns. The dexamethasone suppression test is a valuable biological marker for certain depressions. It may also be useful in identifying subgroups of the schizoaffective disorders, with some schizoaffectives showing an abnormal affective-like response and others not. These and other discriminating biological markers are discussed in this report.
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PMID:Biological markers for the schizophrenic and atypical psychoses. 675 69

The relationship between DSM-III schizophrenia, major affective disorders, and the psychotic disorders not elsewhere classified (PDNEC) can be explored through studies which attempt to determine whether these disorders can be differentiated from one another and normal controls by biological measures. Preliminary results of an ongoing project which utilizes measures of blood platelet monoamine oxidase (MAO), serotonin (5-HT) uptake, and 5-HT content, and the apomorphine-induced increase in growth hormone (GH) to accomplish these goals are reported here. DSM-III major affective disorders (bipolar disorder and major depression) can be differentiated from normal controls by the V max of platelet 5-HT. Platelet 5-HT V max of bipolar disorder, depressed type, is significantly different from that of schizophrenia and PDNEC. Elevated platelet 5-HT content is present in black schizophrenic patients compared to black normal controls. Platelet MAO was increased in a small group of schizophreniform female patients. There was no difference in the apomorphine-induced GH response between any of the diagnostic groups. If confirmed in a larger series of patients, these results tend to identify the PDNEC more closely with schizophrenia than the major affective disorders.
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PMID:Biological studies of DSM-III psychotic disorders. I. Platelet measures and apomorphine-induced growth hormone response. 675 71


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