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 specific and sensitive radioimmunoassay for the determination of 3,4-dimethoxyphenylethylamine (3,4-DMPEA) in urine was developed. In 5 fasting healthy volunteers excretion of 3,4-DMPEA was not diminished, indicating that this substance can be regarded as an endogenous metabolite. In addition, the time profile of the excretion of 3,4-DMPEA was measured in one patient during total fasting. In 25 patients with schizophrenic psychoses, 9 psychiatric patients without schizophrenia and 80 control patients excretion of 3,4-DMPEA was compared. No significant differences could be observed between these three groups.
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PMID:3,4-Dimethoxyphenylethylamine excretion of normals and schizophrenics, behaviour during total fasting. 70 88

Three main biogenic amine hypotheses for the origin of schizophrenia are discussed. The dopamine theory of schizophrenia postulates a pathogenetic connection between the disease and changes in the activity of dopaminergic cells in the brain. The theory is mainly based on findings on the mechanism of action of neuroleptics, on the clinical features and pharmacology of the amphetamine psychosis, and on some amphetamine effects in animals. Several results are in good agreement with the assumption of a state of hyperactivity of central dopamine neurons, whereas others, e.g. the lack of an increased dopamine turnover, are not. According to another theory, schizophrenia is caused by reversible damage to central norepinephrine cells. So far the only empirical basis for this theory is the finding that the activity of dopamine-beta-hydroxylase, a marker enzyme for noradrenaline cells, is lowered in the brains of schizophrenic patients. Thus further confirmation is required. The transmethylation hypotheses assume that hallucinogenic amine metabolites are produced in the body and lead to the appearance of schizophrenic symptoms. Whether or not the occurrence of DMPEA, presumably an oxymethylation product of the dopamine metabolism, is specific for schizophrenics is still open to question; if it is, the meaning of this finding is obscure. Current results leave open the possibility that N-dimethyltryptamine or other N-methylated hallucinogenic biogenic amine metabolites cause the disease; however, this hypothesis is hardly confirmed by positive empirical results.
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PMID:[Biogenic amines and schizophrenia]. 106 94

A quantitative method for the detection of DMPEA in urine was developed. It is based on the fluorometric determination of DMPEA in the form of its phosphopyridoxyl derivate. The limit of detection is 2 microgram DMPEA per 1 g creatinine. The DMPEA content was measured in urine from healthy persons, from schizophrenics, and from psychiatric patients without schizophrenia hospitalized with the schizophrenics. From each person five to ten 24-hr urine samples were investigated. DMPEA could be found neither in schizophrenics nor in controls or healthy persons. Finally, the urinary excretion of parenterally applied 14C-DMPEA was determined in three healthy volunteers and in three rats. In man about 25% of the label was excreted as DMPEA. The main metabolite in urine was homoveratric acid. Both compounds were excreted as conjugates.
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PMID:Quantitative investigation on the urinary excretion and metabolism of 3,4-dimethoxyphenylethylamine in schizophrenics and normal individuals. 705 39