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)

Schizophrenia may be associated with increased prostaglandin synthesis in certain parts of the brain. This hypothesis is based on the following findings: (1) Catalepsy, which is the nearest equivalent in animals to human catatonia, develops in cats when prostaglandin E1 is injected into the cerebral ventricles and when during endotoxin or lipid A fever the prostaglandin E2 level in cisternal c.s.f. rises to high levels; however, when fever and prostaglandin level are brought down by non-steroid anti-pyretics which inhibit prostaglandin synthesis, catalepsy disappears as well. (2) Febrile episodes are a genuine syndrome of schizophrenia.
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PMID:Possible association of schizophrenia with a disturbance in prostaglandin metabolism: a physiological hypothesis. 1 19

It has been proposed that schizophrenia is a prostaglandin-deficiency disease and also that it is a disease of prostaglandin excess. New evidence is reviewed which suggests that 'classic' schizophrenia is due to a specific deficiency of prostaglandin E1 while certain toxic and vitamin-deficiency psychoses may be due to a broader spectrum of prostaglandin deficiency. There is also good evidence that a particular schizophrenic subgroup, which includes catatonic schizophrenia but may not be confirmed to it, is associated with an excess of prostaglandins. Part of the explanation may be that prostaglandin E1 has a 'bell-shaped' dose-response curve with high concentrations having effects similar to those of prostaglandin deficiency.
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PMID:Prostaglandins and schizophrenia: further discussion of the evidence. 63 69

The author presents a hypothesis relating prostaglandin E1 (PGE1) deficiency to schizophrenia. The hypothesis is consistent with the importance of prolactin-stimulating properties in currently used antipsychotic drugs, the effect of prolactin on PGE1 synthesis, and the deficiency of PGE1 regulation in schizophrenic platelets. The author relates the PGE1 deficiency hypothesis to theories implicating dopamine and endorphins in the etiology of schizophrenia. A clinical trial in chronic schizophrenics has suggested the possible therapeutic efficacy of penicillin, a drug without dopamine-blocking actions which can stimulate PGE1 synthesis directly.
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PMID:Dopamine supersensitivity, endorphin excess, and prostaglandin E1 deficiency: three aspects of the same schizophrenic elephant. 73 62

In the context of the dopamine hypothesis of schizophrenia, the authors examined postsynaptic dopamine (DA) receptor sensitivity in schizophrenic patients by means of a neuroendocrine strategy using the DA receptor agonist apomorphine and growth hormone (GH) release as the measurable postsynaptic event. The activity of platelet adenylate cyclase, an enzyme intimately associated with catecholamine receptor activity, was also studied following stimulation by prostaglandin E1 (PGE1). Patients diagnosed as having acute schizophrenia had significantly higher GH responses and adenylate cyclase activity than normal control subjects and patients diagnosed as having chronic schizophrenia. Chronic schizophrenic patients with and without tardive dyskinesia showed GH responses slightly lower than but not significantly different from those of control groups.
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PMID:Postsynaptic supersensitivity in schizophrenia. 84 78

Adenosine diphosphate (ADP) stimulates the synthesis of prostaglandin E1 (PGE1) in lysed platelets from normal subjects, patients with affective illness but not in platelets from cases of schizophrenia. The stimulation is concentration-dependent and follows a curve which is mildly sigmoid in the normal, markedly sigmoid in depression and hyperbolic in mania.
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PMID:Effect of ADP on PGE1 formation in blood platelets from patients with depression, mania and schizophrenia. 120 54

We referred to Borison's method of making the model schizophrenia. Rats were injected d-amphetamine intraperitoneally once a day so that the schizophrenia models were established within four weeks. After five weeks, rats with schizophrenia were treated with chlorpromazine. Contents of plasma prostaglandin E1(PGE1) in rats were determined before and after treatment respectively. This study demonstrated that contents of plasma PGE1 in rats receiving amphetamine for four weeks were higher than those in control animals (P < 0.05). At this time, male rats' stereotypy scores were 3.5 and female stereotypy scores 5. But contents of plasma PGE1 in rats with schizophrenia approached those in control animals with giving amphetamine once a day continuously. Contents of plasma PGE1 decreased in rats with schizophrenia receiving chlorpromazine.
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PMID:[Preliminary study of changes in plasma prostaglandin E1 in rats with experimental "schizophrenia"]. 129 Dec 51

Essential fatty acids (EFAs) and their eicosanoid derivatives are important constituents of the brain and regulators of neuronal function. There is direct and indirect evidence of impaired metabolism of prostaglandin (PG)E1 in schizophrenia. There is also direct evidence of abnormal EFA biochemistry with plasma phospholipids from five populations and brain phospholipids from another all showing reduced levels of linoleic acid and elevated levels of 22-carbon EFAs of both n-6 and n-3 series. Clinical trials of PGE1 and of the PGE1 precursors, gamma-linolenic acid (GLA) and dihomo-gamma-linolenic acid (DGLA) have shown modest therapeutic effects. In view of lack of therapeutic process involving drugs based on the dopamine concept of schizophrenia, it is time for new approaches based on the EFA/PG concept to be evaluated thoroughly.
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PMID:The relationship between schizophrenia and essential fatty acid and eicosanoid metabolism. 132 49

The inhibitory effects of prostaglandin E1 (PGE1) on the platelet aggregation response (PAR) to adenosine diphosphate (ADP) in 103 schizophrenics, 55 patients with other mental disorders, and 71 controls were examined. The three groups did not differ in PAR to ADP. However, schizophrenic patients, especially in the acute state, showed a significant reduction in the inhibitory effects of PGE1 on PAR compared to the other two groups. These results suggest PGE1 hyposensitivity exists in some schizophrenic patients, which may result from PGE1 deficiency. As clinical characteristics of the subgroup showing platelet PGE1 subsensitivity, relatively successful heterosexual relations, less anergia, and a more severe activation factor on BPRS were identified. Furthermore, the relationship between platelet sensitivity to PGE1 and brain morphology, using magnetic resonance imaging on 39 male schizophrenics was examined. Of 11 parameters obtained from MRI measurements, only callosum: brain ratio showed a significant negative correlation with a platelet sensitivity to PGE1. The current study suggested existence of a subgroup of schizophrenia having platelet hyposensitivity and a definite clinical feature as state markers and small corpus callosum as a trait marker.
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PMID:Prostaglandin E1 suppression of platelet aggregation response in schizophrenia. 185 78

The niacin test (oral administration of 200 mg of nicotine acid) was done in 33 schizophrenics and 18 endogenous depressed drug-free patients in the presence of intense symptomatology. The erythema reaction was found in 25 schizophrenics (76%) and in all depressed patients. No significant differences in basal clinical features between schizophrenics with and without erythema reaction were found. The measurements of maximal increase of the left ear lap temperature after nicotine acid administration as well as time needed to note such increase did not show significant differences between schizophrenic patients with and without erythema reaction, and patients with endogenous depression. The results show a limited usefulness of the niacin test in schizophrenia. Nevertheless, the results suggest the possibility that among the small number of schizophrenics there is metabolic defect probably connected with the low activity of PGE1 prostaglandins.
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PMID:[The niacin test in schizophrenia]. 208 15

Several aspects of cyclic AMP second messenger signal generation were examined in EBV-transformed cell lines from 12 schizophrenic patients and 12 age- and sex-matched controls. No evidence was obtained suggesting a heritable abnormality in cyclic AMP synthesis in schizophrenia. Basal, forskolin, A1/NaF- and GppNHp-stimulated cyclic AMP synthesis in membranes from transformed cell lines was identical for schizophrenic and control subjects. In addition, no significant differences were observed for basal, forskolin-, isoproterenol- and prostaglandin E1-stimulated cyclic AMP accumulation in intact cell lines derived from ten of the schizophrenic patients compared with cell lines derived from ten of the control subjects.
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PMID:Cyclic AMP second messenger signal generation in EBV-transformed lymphoblastoid cells from schizophrenic patients. 217 Jun 38


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