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)

The authors assess the results of several studies, fundamental or clinical with therapeutic tests, to demonstrate a possible role of prostaglandins--specially of a possible lack of PGE1--in the pathogeny of certain forms of schizophrenia. The heterogeneousness of the results leads one to think there's heterogeneousness of the illness. Meanwhile, in certain cases, the contribution of a direct precursor of PGE1 the GLA, has given possible noticeable clinical results, mainly with deficiency symptoms.
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PMID:[Prostaglandins E1 and psychopathogeny of schizophrenia]. 226 1

Psychotic disorders, particularly schizophrenia, are associated with clinical phenomena that can be explained by disturbances in polyunsaturated fatty acid and prostaglandin metabolism. Previous studies of PUFA, PG synthesis, PGE1 receptor activity and aggregation responses in platelets, and clinical treatment trials suggest a role for PGE in the pathophysiology of schizophrenia. Since a decrease in PGE1 activity can be associated with an increase of dopamine release, a deficiency of PGE1 is consistent with the dopamine hypothesis of schizophrenia. State-of-the-art assay and clinical trial methodology should clarify the role of PUFA metabolism in schizophrenia.
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PMID:Polyunsaturated fatty acids, prostaglandins, and schizophrenia. 267 45

The inhibitory effects of norepinephrine (NE) on the cyclic adenosine-3',5'-monophosphate (cAMP) response to prostaglandin E1 (PGE1), a measure of alpha 2-adrenergic receptor function, have been compared in platelets from drug-free schizophrenic patients, depressive patients, and normal controls. The absolute value of the inhibition by NE of the cAMP response to PGE1 was smaller in platelets from schizophrenic and depressive patients than in controls. However, this result was secondary to the smaller baseline platelet cAMP response to PGE1 in patients with these disorders. Effects of NE on cAMP production did not discriminate between actively ill and remitted patients with either schizophrenia or depression. Platelet alpha 2-receptor sensitivity, as measured by the effects of NE on cAMP production, does not appear to be altered in these psychiatric disorders.
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PMID:Platelet alpha 2-adrenergic receptor function in psychiatric disorders. 283 62

The postulated deficiency of prostaglandin E1 series (PGE1) in schizophrenia has been investigated in a controlled therapeutic trial. Twenty-one inpatients with a schizophrenic illness resistant to neuroleptic drug treatments were randomly assigned to one of three treatment conditions in a blind controlled trial of dihomo-gammalinolenic acid (DHLA), a PGE1 precursor. Patients received depot neuroleptic medication and DHLA capsules, placebo depot medication and DHLA capsules, or placebo depot medication and placebo capsules. No marked treatment effects were noticed on ratings of the patients' behaviour or symptomatology, though some clinical effects were noted in dyskinetic patients. Abnormalities in red blood cell lipids were observed in the patients entering the trial, suggesting that further investigation of an EFA/prostaglandin deficiency hypothesis in schizophrenia is worth pursuing.
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PMID:A controlled trial of prostaglandin E1 precursor in chronic neuroleptic resistant schizophrenic patients. 287 May 33

Alpha 2-adrenergic receptor function was measured in platelets from chronic schizophrenic patients and normal controls. The number of alpha 2-receptors was greater in patients' platelets, and the prostaglandin E1 (PGE1)-stimulated cyclic AMP (cAMP) production lower, when compared with the normal controls. The changes measured may occur only in the platelet, but if central nervous system neurons share with platelets these changes, one might speculate that an increase in the number of alpha 2-receptors and a decrease in cAMP production may relate to the psychopathology of schizophrenia.
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PMID:Alpha-adrenergic receptors and cyclic AMP production in a group of schizophrenic patients. 301 34

The cyclic adenosine monophosphate (cAMP) responses to prostaglandin E1 (PGE1) in platelets and leukocytes from drug-free schizophrenic patients, depressive patients, and normal controls have been compared. Both schizophrenic and depressive patients had a significantly lower platelet cAMP response to PGE1 than controls. The platelet cAMP response to PGE1 did not discriminate among exacerbated, remitted, and poor-prognosis schizophrenic patients, or between exacerbated and remitted depressive patients. The cAMP response to PGE1 was negatively correlated with global symptom severity in actively ill schizophrenic patients, but was not correlated with symptom severity in exacerbated depressive patients. The leukocyte cAMP response to PGE1 did not differ among normal controls, schizophrenic patients, and depressive patients. These data indicate that a diminished platelet cAMP response to PGE1 may be a marker common to both schizophrenia and depression but that this effect does not extend to a cAMP-linked PGE1 receptor on another blood cell type.
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PMID:Prostaglandin receptor sensitivity in psychiatric disorders. 301 69

The authors refer to the biochemical investigation of the occurrence and metabolism of essential fatty acids in the CNS and to significant differences in results between those obtained in animal experiments and those involving human beings, taking into account hypotheses that have not yet met with general acceptance. Discussed is the possible connection between eicosanic acid and schizophrenia, notably Horrobin's hypothesis of PGE1 deficiency in schizophrenic patients. The probability of a pathogenetic connection between changes in the metabolism of fatty acids and the occurrence of endogenous psychoses is assumed.
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PMID:[Prostaglandins and endogenous psychoses]. 378 74

alpha-Adrenergic receptor function was assessed in platelets from drug-free schizophrenic patients and control subjects. The number of alpha-receptors was similar in platelet membranes from schizophrenic patients and control subjects. In intact platelets from schizophrenic male, but not female, patients, prostaglandin E1 (PGE1)-stimulated cyclic adenosine monophosphate (cAMP) level was less than in control subjects. This defect may be due, at least in part, to decreased adenylate cyclase activity. In platelet lysates from schizophrenic patients, but not from normal control subjects, adenylate cyclase activity was diminished and PGE1-stimulated adenylate cyclase activity could be restored partially by the addition of guanosine triphosphate. Treatment with neuroleptic drugs or lithium carbonate did not change alpha-receptor number or cAMP production in platelets from schizophrenic patients, but high doses of propranolol hydrochloride increased cAMP production without affecting the number of alpha-receptors. If the production of cAMP in neurons is similar to that in platelets, diminished cAMP production may be associated with a vulnerability to schizophrenia.
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PMID:alpha-Adrenergic receptor function in schizophrenia. Receptor number, cyclic adenosine monophosphate production, adenylate cyclase activity, and effect of drugs. 613 56

1. Clinical observations and experimental findings are rendered which have raised the possibility that schizophrenia may be related to PGE deficiency and/or excess. 2. In favor of PGE1 deficiency are the findings that ADP-induced increase in synthesis and PGE1 stimulated cAMP accumulation are significantly lower in platelets of schizophrenic patients than in normal controls. 3. In favor of PGE excess are the findings that the concentration of immunoreactive PGE in cerebrospinal fluid of schizophrenics is higher than that of healthy controls, neurotic patients and patients undergoing neurological examination. 4. An argument against the PG excess hypothesis is that paracetamol, a substance which reduces PG levels has no therapeutic effect in schizophrenia. 5. The two hypotheses--PGE deficiency and PGE excess--are not compatible because of the bell shape dose response curve with PG's in certain biological systems.
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PMID:Prostaglandins and schizophrenia: a review. 628 32

Recently, increased brain and spinal fluid (CSF) norepinephrine (NE), and a decreased cAMP response to prostaglandin E1 (PgE1) stimulation of platelet NE sensitive adenylcyclase were observed in some schizophrenic patients. Low CSF dopamine-beta-hydroxylase (DBH) activity was related to brain atrophy, whereas high plasma DBH was associated with tardive dyskinesia. Increased NE (in brain and CSF) and 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels and decreased plasma DBH activity in the brain were associated with a diagnosis of paranoid schizophrenia. Impaired NE transmission in schizophrenia may relate to disturbances in the autonomic nervous system, deficits in attention and information processing and to an impaired ability to deal with stress. Although pharmacological studies have suggested a major role for dopamine (DA) in schizophrenic psychosis, this review indicates the need for further exploration of the NE system. Future studies should address the relationship with DA, the autonomic nervous system (ANS), cerebral blood flow, brain metabolism, stress response, negative and prodromal symptoms.
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PMID:Impaired noradrenergic transmission in schizophrenia? 632 3


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