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)

3,4-Dihydroxy-5-fluorophenylalanine, fluorodopa, was injected into rats in which unilateral lesions of the nigrostriatal pathway had been made. The rats rotated towards the side with the lesions, thus providing further evidence that fluoro-dopa is an analogue of dopa. [(18)F]Fluoro-dopa was then injected intravenously into fully conscious baboons. A well-collimated scintillation detector, aligned along the occipitomental axis, recorded the accumulation of (18)F in the brain. Control animals accumulated (18)F continuously for 100 min. This accumulation represents net transport of [(18)F]fluoro-dopa from blood to brain, decarboxylation to [(18)F]fluoro-dopamine, storage, and degradation of [(18)F]fluoro-dopamine. alpha-Methyl-dopa, a competitive inhibitor of dopa transport and decarboxylation, prevented the accumulation of (18)F; reserpine, known to release stored intracerebral dopamine, discharged (18)F; pargyline, a monoamine oxidase inhibitor, and haloperidol, a known augmentor of intracerebral dopamine turnover, increased the rate of accumulation of (18)F. These changes in the accumulation of intracerebral (18)F, after [(18)F]fluoro-dopa, were commensurate with the known action of the drugs used to induce them and demonstrate the use of a gamma-emitting precursor of a neurotransmitter to monitor simply, atraumatically, and externally the intracerebral metabolism of the transmitter in fully conscious primates. When applied to man, the same technique should be able to provide more conclusive evidence than is presently available for the role of catecholamines in schizophrenia and depression. It should also provide further insight into the natural history of nigrostriatal diseases and the action of drugs used in their treatment.
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PMID:[18F]fluoro-dopa, an analogue of dopa, and its use in direct external measurements of storage, degradation, and turnover of intracerebral dopamine. 41 9

Conflicting reports on the association between platelet MAO activity and schizophrenia prompted a critical review and determinations on identical samples at one laboratory in Sweden and one in the U.S.A. Samples originated from eight schizophrenics and 27 relatives belonging to a large pedigree, thus ensuring biological homogeneity. In the USA laboratory, a significantly lower MAO activity was found in the schizophrenics when benzylamine or beta-phenylethylamine was used as substrate (but not with tryptamine), while a similar result was obtained in the Swedish laboratory when tryptamine was used (but not with benzylamine or beta-phenylethylamine). Comparisons between materials examined in different laboratories do not seem meaningful until differences in methodologies have been clarified. At present there is neither proof nor disproof of MAO being a "genetic marker" for vulnerability to the schizophrenic disorder.
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PMID:Platelet monoamine oxidase in a pedigree with schizophrenia: an interlaboratory project. 43 26

Individuals potentially at risk for psychiatric disorders were identified by screening 375 college student volunteers for low platelet monoamine oxidase (MAO) activity levels. The lower and upper 10% in MAO activity were administered a personal and family history interview, psychological tests and average evoked response (AER) electroencephalographic procedures. Results indicated that low MAO males and females were socially more active, had more psychiatric contact, and had relatives who were psychiatrically more disturbed than high MAO subjects. Low MAO males had more convictions, experimented more with illegal drugs and had elevated scores on the MMPI. AER criteria further defined a high risk group of low MAO-AER augmenters which had more suicides among their relatives and higher scores on the schizophrenia scale of the MMPI.
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PMID:Platelet MAO activity and evoked potentials in the identification of subjects biologically at risk for psychiatric disorders. 44 87

Lower monoamine oxidase (MAO) levels are reported in the blood platelets from chronic schizophrenics than in normal controls. Attempts to replicate these findings in other laboratories have been unsuccessful thus contradicting the suggestion that low MAO activity is a genetically determined biological factor in schizophrenia. We now present evidence to show that the endogenous amines present in platelets (serotonin) react non-enzymatically with the highly reactive aldehyde produced by MAO and thereby reduce the extractable radioactivity in the radiometric assays for MAO. Various biogenic amines such as serotonin, dopamine and m-tyramine were tested for their interference by adding them in nanomolar concentrations to incubation mixtures containing platelet samples or partially purified rat liver MAO and (14C-)p-tyramine or phenethylamine as substrates. The amines were added before, during and after incubation. In all three cases the apparent inhibition by each amine was the same, the percent inhibition depending on the structure of the amine.
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PMID:Interference by endogenous amines in the determination of monoamine oxidase activity of human platelet samples. 45 49

Platelet monoamine oxidase (MAO) activity in 10 normal volunteers was studied as a function of platelet protein or electronically-determined platelet counts. Comparisons of the two methods were made for samples assayed on the same day as well as one week later. The MAO activities resulting from both methods were significantly correlated and reproducible but the results of the platelet count method were, in most instances, slightly but significantly more reliable than the platelet protein method. The relevance of these results to the controversy concerning platelet MAO activity in schizophrenia is discussed.
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PMID:Comparison of platelet count and platelet protein methods for determination of platelet MAO activity. 47 56

Two studies were undertaken to verify the presence of lowered platelet monoamine oxidase activity in chronic schizophrenia. In the first study, a retrospective chart analysis, the mean platelet activity of patients with chronic schizophrenia (7.73+/-0.64 nmol of benzylaldehyde product per 10(8) platelets per hour [S.E.M.]) differed significantly from that of normal controls (12.13+/-0.2, P less than 0.001). Chronic paranoid schizophrenics (4.81+/-0.46) differed significantly from chronic nonparanoid schizophrenics (8.6+/-0.75, P less than 0.03). A separate prospective study confirmed significantly lower values for monoamine oxidase activity in chronic schizophrenic patients diagnosed as paranoid (5.97+/-1.17) or as having secondary paranoid features (6.28+/-0.71) as compared to chronic nonparanoid schizophrenics (9.81+/-0.87, P less than 0.001). Chronic paranoid schizophrenia may be a separate disorder from the other chronic forms of schizophrenia, and this difference may be related, at least in part, to biochemical characteristics.
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PMID:Are paranoid schizophrenics biologically different from other schizophrenics? 61 36

This study replicates and extends earlier work by finding that low levels of platelet monoamine oxidase (MAO) activity correlate with sensation seeking, high ego strength, positive affect, and high leisure time activity levels, somewhat similar psychological correlates also being found for plasma amine oxidase activity. Although there are several ways in which a schizophrenia/MAO relationship may exist and still be congruent with the present data, these results pose difficulties for theories which link low MAO activity levels specifically to schizophrenia. Nothing in the present findings, however, is incongruent with the possibility of an association between low platelet MAO activity and bipolar affective disorder.
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PMID:Psychological correlates of monoamine oxidase activity in normals. 64 36

Rheumatoid arthritis and schizophrenia have been described in early surveys as mutually exclusive disorders. Such claims are seen as especially interesting in view of: (1) indications that both illnesses often follow prodromes of severe psychological stress, (2) theories regarding hypermethylation of indoleamines producing endogenous psychotogens in schizophrenia, and (3) studies of rheumatoid arthritis reporting excessive binding of L-tryptophan to plasma protein, abnormalities of urinary tryptophan metabolites, decreased serotonin binding capacity of thrombocytes, and decreased MAO activity in joint fluid. Further comparative studies of tryptophan metabolism in schizophrenia and rheumatoid arthritis might enhance knowledge of pathogenesis in either or both diseases.
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PMID:Schizophrenia, rheumatoid arthritis and trytophan metabolism. 65 73

The authors measured the monoaminoxidase activity in thrombocytes of 28 schizophrenic patients and in 36 normal donors. The monoamine oxidase activity in schizophrenic patients was decreased by 14% and in the subgroup of patients with continuous schizophrenia by 19.5% as compared to that of normals. The monoamine oxidase activity in schizophrenic female patients did not significantly differ from the norm, while the male patients differed highly significantly from the normal. The decrease of monoamine oxidase activity correlated with the level of negative disorders (r = 0,71; P less than 0,01). A correlation with positive disorders was not noted.
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PMID:[Decrease in the thrombocyte monoamine oxidase activity of schizophrenic patients]. 70 10

The urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG) and other catecholamine metabolites was measured in a series of 63 patients with various clinically defined subtypes of depressive disorders. MHPG excretion was significantly lower in patients with bipolar manic-depressive depressions and schizo-affective depressions than in patients with unipolar nonendogenous depressions. Patients with schizophrenia-related depressions also excreted reduced levels of MHPG when compared with patients with unipolar nonendogenous depressions. Moreover, levels of urinary epinephrine and metanephrine were significantly lower in patients with schizophrenia-related depressions. These data, coupled with our recent finding that patients with schizophrenia-related depressions had significantly higher levels of platelet monoamine oxidase activity than control subjects of patients with unipolar endogenous depressions, suggest that we can discriminate three biochemically discrete subgroups of depressive disorders corresponding to the following clinically defined subtypes: (1) the bipolar manic-depressive depressions plus the schizo-affective depressions; (2) the unipolar nonendogenous depressions; and (3) the schizophrenia-related depressions.
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PMID:Toward a biochemical classification of depressive disorders. I. Differences in urinary excretion of MHPG and other catecholamine metabolites in clinically defined subtypes of depressions. 72 78


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