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 significant increase of cerebrospinal fluid (CSF) noradrenaline (NA) levels, probably reflecting a rise of central noradrenergic activity, has been observed in a sample of acute schizophrenic patients as compared with a population of subjects without personal or family history of major psychoses. CSF NA levels have been found to be significantly correlated with computerized EEG (C-EEG) indicators of arousal (negative correlation with alpha relative activity and positive correlation with alpha barycentric frequency and beta relative activity in frontal and central leads). No significant relationship has emerged between CSF NA concentration and psychosis ratings on CPRS as well as platelet MAO activity. These findings seems to confirm the link between central noradrenergic hyperactivity and the condition of enhanced arousal of the schizophrenic patient, although the role of this condition in the pathophysiology of schizophrenia (primary phenomenon or non-specific consequence of the stress related to the illness?) remains to be elucidated.
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PMID:Relationship between CSF noradrenaline levels, C-EEG indicators of activation and psychosis ratings in drug-free schizophrenic patients. 396 38

Whole blood serotonin and platelet monoamine oxidase (MAO) activity in boys with schizophrenia, schizotypal personality disorder, or major depressive disorder was compared with that of boys serving as controls. Boys with schizophrenia and schizotypal personality disorder had significantly higher platelet MAO than boys with major depressive disorder or controls. Boys with major depressive disorder had lower whole blood serotonin than boys with schizophrenia or schizotypal personality disorder.
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PMID:Comparison of whole blood serotonin and platelet MAO in children with schizophrenia and major depressive disorder. 397 62

Platelet monoamine oxidase (MAO) has been implicated in the biology of several psychiatric disorders, including schizophrenia. Genetic factors contribute to the variance of MAO activity; however, its mode of inheritance is unknown. To assess the distribution and familial patterns of platelet MAO activity, we studied 73 chronic schizophrenic patients and 219 of their first-degree relatives. The activity distribution was skewed and admixture of two distributions gave a better fit to the data than a single distribution. Single-major-locus hypotheses were tested by pedigree analysis methods for quantitative traits. Using the transmission probability model, the familial transmission of MAO activity was consistent with either recessive or additive inheritance but not with dominant inheritance; the environmental hypothesis was strongly rejected. No effect of genotype on probability of illness was observed suggesting no relationship between the particular major locus tested and schizophrenia. The implications for genetic research in schizophrenia were discussed.
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PMID:Genetic analysis of platelet monoamine oxidase activity in families of schizophrenic patients. 398 38

The content of SH-groups and substrate specificity have been studied in purified preparations of monoamine oxidase (MAO) from human brain. It has been shown that both in schizophrenic and mentally normal persons MAO occurs in a partially oxidized state. The enzyme contains 2 SH-groups per 10(5) daltons of protein and deaminates MAO substrates (serotonin, beta-phenylethylamine) along with histamine, diamine oxidase substrate. Reduction of the partially oxidized SH-groups of MAO in schizophrenics up to 15 SH-groups per 10(5) daltons of protein (the normal value for human brain MAO) does not eliminate the histamine deaminase activity as is the case in experiments with MAO from the normal brain but, on the contrary, considerably potentiates it. The data suggest certain structural alteration of MAO in schizophrenia.
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PMID:[Brain monoamine oxidase in schizophrenia]. 401 56

Among 76 chronic schizophrenic patients, plasma amine oxidase activity was unrelated to paranoid/nonparanoid subtype, narrow/broad diagnostic criteria, prognosis, or age at onset. These clinical indices do not identify biological subtypes of schizophrenia with deviant plasma amine oxidase activity.
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PMID:Plasma amine oxidase and clinical features of schizophrenia. 402 99

Monoamine oxidase specific activities and molecular turnover numbers have been measured in families with at least two schizophrenic members. Neither measure of monoamine oxidase was different in schizophrenics compared with their first degree relatives. Molecular turnover number was remarkably similar in males and females and when the group was considered by age, diagnosis, drug status and family membership. Neither specific activity nor turnover number could be used in risk estimation for the development of schizophrenia in members of these families.
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PMID:Platelet monoamine oxidase: specific activity and turnover number in schizophrenics and their families. 406 35

The establishment of the new diagnostic category, Schizotypal Personality Disorder (SPD), has stimulated biological studies of patients with this disorder. Such studies offer the potential of better understanding the diagnosis and treatment of SPD as well as more clearly defining the boundaries of the schizophrenic disorders. SPD has been studied in the clinical setting, in family studies of schizophrenia, and in the biological high-risk paradigm. In most cases, biological variables associated with schizophrenia have been evaluated. Decreased activities of plasma amine oxidase and platelet monoamine oxidase have been associated with SPD in the families of schizophrenics and in "biological high-risk" studies. Smooth pursuit eye movement (SPEM) impairment has also been associated with SPD in a "biological high-risk" study of college students. Inferior backward masking performance has been demonstrated in SPD patients in the clinical setting. Other studies using psychophysiological measures have been applied to subjects with psychological characteristics similar to DSM-III SPD and found biological abnormalities similar to those reported in schizophrenia. These studies are consistent with the possibility that some individuals with SPD may share common psychobiological abnormalities with schizophrenic individuals and may sharpen our understanding of SPD and its relationship to schizophrenia.
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PMID:Biological markers in schizotypal personality disorder. 408 50

Monoamine oxidase activity in blood platelets was measured, with [(14)C]tryptamine as substrate, in 13 monozygotic twin pairs discordant for schizophrenia and in 23 normal volunteers. The monoamine oxidase activity of both schizophrenic and nonschizophrenic co-twins was significantly lower than it was for the normals, and it was highly correlated between twins. In addition, there was a significant inverse correlation between a measure of the degree of the schizophrenic disorder and the monoamine oxidase activity. These data suggest, but do not prove, that reduced platelet monoamine oxidase activity may provide a genetic marker for vulnerability to schizophrenia.
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PMID:Reduced monoamine oxidase activity in platelets: a possible genetic marker for vulnerability to schizophrenia. 468 89

The level of platelet monoamine oxidase (MAO) has been found to be abnormally low in certain types of schizophrenia and in a number of other pathological conditions. It has been suggested that MAO in platelets may be a genetic marker for a subgroup of patients with schizophrenia; however, we have demonstrated that several nongenetic factors influence platelet MAO activity by affecting the platelet rather than the MAO enzyme protein. We have observed platelet MAO activities to be heterogeneously distributed in a given subject's platelet population, heavy platelet fractions having significantly higher specific activity than light platelet fractions. We have also found platelet MAO activity to be significantly correlated with mean platelet volume, platelet protein densities, and protein content per platelet. These changes, which might be induced by drugs and stress, could modify production, mobilization, and clearance of platelets and, hence, influence apparent MAO activity.
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PMID:Platelet monoamine oxidase as a function of nongenetic factors. 610 76

The most widely replicated neurochemical finding in schizophrenia is that of lower levels of monoamine oxidase (MAO) in the platelets of chronic schizophrenics than in normal controls. Yet, the etiological role of MAO in schizophrenia remains to be demonstrated. The incidence of low MAO in other psychiatric disorders, effects of diet, hormones and drugs, and relationships of platelet MAO to brain levels and genetic mechanisms remain unclear. This article examines factors which make any biological indicator suitable for use as a diagnostic test for schizophrenia and inquires into the methodological pitfalls and unexamined assumptions of various research strategies which use this measure.
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PMID:Schizophrenia and platelet monoamine oxidase: research strategies. 610 78


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