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)

Inhibition of central dopamine functions appears to be a common basic property of antipsychotic drugs. The mesolimbic and nigrostriatal portions of the dopaminergic system are probably the main targets of these drugs for the mental and the extrapyramidal actions respectively. Dopaminergic hyperfunction, induced by amphetamines or dopa, may lead to a disturbance mimicking paranoid schizophrenia, lending further support for a key role of dopamine in mental functions. While a primary disturbance in dopamine function in schizophrenia cannot be ruled out, the intimate relationship between dopaminergic and other neuronal systems must be emphasized. The possible involvement of other amine, aminoacid or peptide transmitters in schizophrenia cannot be disregarded.
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PMID:Does dopamine play a role in schizophrenia? 2 90

Inhibition of central dopamine functions appears to be a common basic property of antipsychotic drugs. The mesolimbic and nigrostriatal portions of the dopaminergic system are probably the main targets for the mental and the extrapyramidal actions, respectively, of these drugs. The fact that dopaminergic hyperfunction induced by amphetamines or dopa may lead to a disturbance mimicking paranoid schizophrenia lends further support for a key role of dopamine in mental functions. Although a primary disturbance in dopamine function in schizophrenia cannot be ruled out, the intimate relationship between dopaminergic and other neuronal systems must be emphasized. The possible involvement of other amine, amino acid, or peptide transmitters in schizophrenia cannot be disregarded.
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PMID:Antipsychotic drugs, neurotransmitters, and schizophrenia. 2 84

There is considerable similarity between paranoid schizophrenia and psychoses provoked by dopaminergic overstimulation in the central nervous system. The fact that neuroleptics are able to block dopaminergic neural activity has led to the hypothesis that there might exist a common biochemical substrate for schizophrenia and e. g. the amphetamine psychoses. Dopaminergic overstimulation may be elicited by different drugs interacting with the dopamine metabolism e. g. dopamine-beta-hydroxylase inhibition (disulfiram, fusaric acid); monoamine-oxidase-inhibition (phenelzine, tranylcypromine); dopamine release (amphetamine); stimulation of postsynaptic dopamine receptors (bromocriptine, apomorphine). Resulting psychotic symptoms consist of ideas of reference, delusions, visual and acustic hallucinations in a clear setting of consciousness. Psychoses occur usually in subjects, who have suffered from various psychiatric illnesses, which have apparently in common a reduced monoamine-oxidase activity in platelets. It is concluded from various biochemical findings, that psychoses resulting from dopaminergic overstimulation and schizophrenia have different biological substrates.
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PMID:[Psychotropic drugs as tools for clinical research into schizophrenia (author's transl)]. 2 31

The model psychosis associated with amphetamine overdosage is known to bear a close resemblance to acute paranoid schizophrenia. Amphetamine is chemically similar to the endogenous sympathomimetic amine, phenylethylamine, which possess many of its pharmacological properties. It is suggested that some cases of schizophrenia may be associated with an abnormal phenylethylamine response, either from increased concentrations of the amine or from abnormal receptor sensitivity to it.
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PMID:Does phenylethylamine cause schizophrenia? 5 86

The antipsychotic actions and extra-pyramidal side-effects of neuroleptic drugs are strongly correlated with their ability to block central dopaminergic transmission. It is argued that the former are more closely related to actions on dopaminergic mechanisms in the "mesolimbic dopamine" system, and the latter to similar actions in the striatum. Although the amphetamine psychosis closely resembles paranoid schizophrenia and may be due to excess dopamine release, clinical, biochemical, and endocrine studies suggest that dopaminergic overactivity is not a necessary concomitant of schizophrenic illnesses. It is suggested that the primary defect in schizophrenia does not lie in the dopamine neuron. It remains to be excluded that the receptors, particularly in the mesolimbic dopamine areas, become supersensitive, or that there is a deficit in a system which normally acts in antiagonism to the to the mesolimbic dopamine system.
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PMID:Dopamine and schizophrenia. 6 Jun 35

A nonselective group of 971 schizophrenic patients was studied. The development of the disease in these patients was characterized by the prevalence of hallucinative disorders during the whole duration of the disease. This group totalled 19.1% of the whole population of patients. The cases with continuous paranoid schizophrenia totalled 42.4% of the studied group (8.1% of the population). The rest observations formed the continual range between paranoid and attack-like schizophrenia.
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PMID:[Prevalence and chief variants of the course of schizophrenia with a predominance of delusional and hallucinatory-delusional disorders throughout the course of the disease (clinico-epidemiologic study)]. 48 40

Monoamine oxidase (MAO) activity has been measured in the platelets of controls (n = 42) and schizophrenic patients (n = 49) of three subtypes, using beta-phenylethylamine, p-tyramine, and tryptamine as substrates. Characteristic differences of MAO activity were observed between platelets of patients and controls; the differences were substrate-typic: decreased enzyme activity was found with all three substrates in platelets of the parnaoid subtype. With tryptamine, MAO activity was decreased in the platelets of all three sub-types of schizophrenia. With p-tyramine, MAO was low in patients with affective psychoses and paranoid schizophrenia. The value of MAO activity measurements as a means for distinguishing sub-types of schizophrenic disorders is improved by using two substrates; tryptamine and p-tyramine. Possible mechanisms of the substrate-typic changes of platelet MAO activity in schizophrenia are discussed.
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PMID:Substrate-typic changes of platelet monoamine oxidase activity in sub-types of schizophrenia. 60 5

The distribution of HLA-A-, B- -and -C-locus antigens was tested in 200 male patients with final diagnosis of schizophrenia. A significant increase of HLA-A28 and HLA-Cw4 antigens and haplotype A10--B18 was found. Indications were obtained for the increase of HLA-A1 in hebephrenic patients. It was presumed that the increase of CW4 represents the common denominator of the diverse findings on paranoid schizophrenia. The increase of CW4 indicates that the paranoid schizophrenia disease susceptibility locus is either the C locus itself or another closely linked locus (or loci). This would stress the importance of the HLA 'central' regions for HLA and disease associations. A hypothesis is presented which points to the possibility that HLA antigens could be genetic markers of three ethiopathogenetic subgroups of schizophrenia. The possible tests of this hypothesis are also suggested.
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PMID:HLA antigens as possible markers of heterogeneity in schizophrenia. 69 Apr 74

Paranoid symptoms were found in 40% of patients admitted to a university general hospital psychiatric unit during a ten-month period. Fifty-eight percent of this group had frank paranoid delusions, while the rest had ideas of reference or generalized suspiciousness. Only one half of those who had paranoid delusions had paranoid schizophrenia. A significant number had affective disorders or organic brain disorder. Ideas of reference and suspiciousness were found in many patients who were not psychotic. The therapeutic implications of these findings are reported in three patients who were inadequately treated for affective disorders because the presence of paranoid symptomatology had led to an incorrect diagnosis of schizophrenia.
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PMID:Paranoid symptoms in patients on a general hospital psychiatric unit. Implications for diagnosis and treatment. 72 91

When studying 750 psychiatric in-patients with psychoses of various diagnostic groups, the symptoms of voice sensations and vibration feelings could only be found among patients with paranoid schizophrenia. In addition, these symptoms were located exclusively in body areas that are involved in the peripheral motor production of voice and speech (areas of head, throat, thorax). In 11 of 15 such cases that could be identified, the sensations of voices and vibrations occurred simultaneously and in identical body parts; in the remaining 4 cases only voices without vibration sensations were reported. Therefore these symptoms can be considered as highly specific for schizophrenia. According to the terminology of Bleuler these two symptoms are because of their rareness to be taken as accessoric symptoms; according to the terminology of Kurt Schneider they have the value of first rank symptoms because of their highly diagnostic specifity for schizophrenia. The pathogenesis of these symptoms is on the one hand discussed under the perspective of language development and the changing function of language for behaviour control; on the other hand, the pathogenesis of these symptoms is discussed from the viewpoint of cybernetic, or neurophysiological-neuroanatomical foundation of speech production and speech control. Both models of explanation have in common that the ideational component of speech is noticed as acustic halluzinations and the motor proprioceptive part of speech is noticed as sensation of vibrations, both in a typically schiphrenic manner, i.e. dissociated and ego-alienated.
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PMID:[Voice and vibration sensations in the speech forming organs: clinical and theoretical aspects of rare symptoms specific for schizophrenia]. 75 82


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