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)

During a drug-free period a group of schizophrenic subjects (N = 9) showed normal mean basal plasma ACTH and cortisol levels in association with normal plasma ACTH and cortisol responses to an infusion of corticotropin-releasing hormone (CRH). Administration of fluphenazine had no effect on basal ACTH and cortisol levels or their responses to CRH (N = 8). These data differ from those previously reported in depressed patients, who showed elevated basal cortisol values in association with a blunted ACTH response to CRH, and add to a growing body of literature which suggests that hypothalamic-pituitary-adrenal regulation is less disturbed in schizophrenia than in depression.
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PMID:The corticotropin-releasing hormone stimulation test in chronic schizophrenia. 302 12

We evaluated ceruletide, a cholecystokininlike peptide, in a double-blind, placebo-controlled study of 20 male chronic schizophrenic patients. After baseline investigations, 10 patients received 0.3 microgram/kg body weight ceruletide, and 10 patients received placebo (normal saline) intramuscularly once weekly for 3 consecutive weeks. Psychopathology was rated on the Brief Psychiatric Rating Scale and the Nurses' Observation Scale for Inpatient Evaluation. Blood was drawn on the same days for estimation of norepinephrine, epinephrine, beta-endorphin, cortisol, and prolactin. There were no significant changes in biochemical parameters. With regard to psychopathology, no significant differences in behavioral ratings were found between the ceruletide- and placebo-treated groups. Furthermore, there was no changes in either positive or negative symptoms of schizophrenia secondary to ceruletide. Contrary to uncontrolled studies, we failed to show antipsychotic properties of ceruletide.
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PMID:A double-blind study with ceruletide in chronic schizophrenic patients: biochemical and clinical results. 353 6

Biologically active peptide fragments derived from the proteolytic cleavage of beta-endorphin (beta E) have been shown to be present in the brain. Based on clinical results using some of these fragments in neuropsychiatric disease studies we investigated the in vitro metabolism of beta E by twice-washed membrane homogenates of postmortem putamen from sex and age matched controls versus subjects with a diagnosis of schizophrenia. The present study demonstrates that frozen (-80 degrees C) postmortem human tissues are viable for these studies and that metabolism in control tissue proceeds similarly to fresh tissues. Furthermore, a significant increase in the formation of the putative neuroleptic-like peptide fragment des-enkephalin-gamma-endorphin in postmortem schizophrenic putamen versus controls was shown. A significant decrease in the formation of beta E was also reported. These data suggest that an approach using postmortem human brain is possible in studying beta-endorphin catabolism and is therefore applicable to other neuropeptide systems.
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PMID:Differential in vitro metabolism of beta-endorphin in schizophrenia. 608 62

In this article the biological factors i.e. neuropathological/structural and biochemical, involved in the pathogenesis of schizophrenia are reviewed. Particularly the endorphin hypothesis, which states that disturbances in the fragmentation of beta-endorphin are implicated in schizophrenia, is emphasized. The concept of type I and type II schizophrenia, disturbances in the serine-glycine metabolism and the neuropeptide strategy are currently under investigation.
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PMID:[Biological determinants of schizophrenic psychoses]. 608 15

The evidence for stress activation of endorphinergic systems suggests a physiological role in endogenous analgesic and anti-anxiety regulation which would provide a reserve in emergency situations. The possibility of involvement of these systems in psychiatric illness arises from the psychotogenic and anxiolytic properties of some opiates. The endorphin-excess and -deficiency hypotheses of schizophrenia are reviewed in the light of naloxone's small but statistically significant antipsychotic action, and the activation of endorphinergic systems in the course of neuroleptic therapy. The hypothesis that endorphinergic deficiency may be present in endogenous depression is reviewed. Although alterations in beta-endorphin immunoreactivity measured peripherally and in CNS have not been substantiated, therapeutic trials using a mu-receptor agonist have shown promise of a rapidly-acting antidepressant effect. ECT is accompanied by increases in plasma beta-endorphin immunoreactivity.
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PMID:Endorphins in psychiatry. 609 Oct 98

This article comprises a systematic ans schematic survey of neuroleptics and antidepressants, their mode of action in the central nervous system, indications and side-effects. Psychic disorders in the aged may be due to anatomical cerebral lesions, but they may be also "functional'. Both types of disorders are concisely described. The possibilities and limitations of treatment with psychotropic drugs are reviewed and special attention is given to the specific problems of this type of therapy in patients of advanced age. It is pointed out that psychic disorders in the aged are multiconditional and that psychopharmacotherapy is just one component of the treatment. The neuropeptide concept is described. The putative clinical significances of neuropeptides derived from ACTH, vasopressin and beta-endorphin (e.g. DTgammaE) are mentioned with respect to learning- and memory processes and schizophrenia.
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PMID:[Mechanism of action and indications for psychopharmaceutic agents; possibilities and limitations in the elderly]. 611 93

Des-tyr1-gamma-endorphin (DT gamma E) was administered intramuscularly in a dose of 1 mg/day for 10 days to 18 neuroleptic-free schizophrenic patients in a double-blind crossover design. Six patients showed either a slight or no antipsychotic response; seven patients showed a moderate antipsychotic response; and the remaining five patients showed a marked antipsychotic response. DT gamma E led to a decrease of plasma prolactin levels in patients treated with DT gamma E in the first period of experimental treatment as compared to those treated with placebo. Neither plasma levels of growth hormone and cortisol nor cerebrospinal fluid concentrations of homovanillic acid, 5-hydroxyindoleacetic acid, and 3-methoxy-4-hydroxyphenylglycol were affected by DT gamma E. Patients suffering from a hebephrenic or paranoid type of schizophrenia and those presenting relatively fewer negative symptoms were most susceptible to treatment with DT gamma E. These data confirm and extend previous findings that DT gamma E has antipsychotic properties in a number of schizophrenic patients.
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PMID:Clinical, biochemical, and hormonal aspects of treatment with Des-tyr1-gamma-endorphin in schizophrenia. 620 51

Since the discovery of the endorphins, several hypotheses have been formulated concerning their involvement in the pathogenesis of schizophrenia. In this article, the hypothesis concerning disturbances in the fragmentation of beta-endorphin is mentioned with special reference to the antipsychotic properties of gamma-type endorphins.
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PMID:[Endorphins of the gamma type in the treatment of schizophrenic psychoses]. 620 7

To elucidate the significance of beta-endorphin in human cerebrospinal fluid (CSF), CSF levels of beta-endorphin-like immunoreactivity (beta-EP-LI) in various diseases were determined by a specific radioimmunoassay and compared with simultaneously determined ACTH-like immunoreactivity (ACTH-LI) levels in CSF. CSF beta-EP-LI and ACTH-LI in the control group, consisting of 5 normal subjects and 19 patients with nonendocrine diseases, were 22.2+/-1.3 and 14.6+/-0.4 fmol/ml, respectively. CSF levels of these peptides in patients with schizophrenia (n = 19) and acromegaly (n = 10) were not significantly different from those in the control group. Patients with Cushing's disease (n = 7) had significantly lower CSF beta-EP-LI and ACTH-LI levels than those in the control group. Four of them showed a parallel increase in CSF beta-EP-LI and CSF ACTH-LI levels after the complete removal of pituitary microadenomas (P < 0.05). Gel chromatography of CSF beta-EP-LI from a normal volunteer, a control patient, and one patient each with catatonia, Nelson's syndrome, Cushing's syndrome (adrenal adenoma), and acromegaly gave similar patterns consisting of three peaks with the elution positions comparable to those of authentic beta-endorphin, beta-lipotropin, and possibly their precursor molecule. Gel chromatographic patterns of CSF beta-EP-LI and ACTH-LI were compared in a normal volunteer. The first peaks of beta-EP-LI and ACTH-LI eluted at the same position and the second peak of ACTH-LI coincided with the elution position of authentic ACTH.CSF beta-EP-LI and ACTH-LI levels determined every 5 min over a period of 80 min in three normal volunteers did not show moment-to-moment variability.A significant correlation (r = 0.75, P < 0.001) was seen between CSF beta-EP-LI and ACTH-LI levels in normal subjects and patients studied (n = 73). This suggests that beta-endorphin and ACTH in human CSF share the common regulatory mechanism in normal and pathologic conditions.
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PMID:Immunoreactive beta-endorphin and adrenocorticotropin in human cerebrospinal fluid. 625 11

The response of plasma beta-endorphin (ir) to infusions of randomly assigned d-amphetamine (20 mg) and placebo was studied in eight schizophrenic patients. Although there was no statistically significant difference between the response to d-amphetamine and placebo, significant increases in plasma beta-endorphin (ir) levels were observed following each infusion. Although heterogeneity in beta-endorphin (ir) response was observed, individual differences did not relate to clinical variables such as abnormalities on computed tomography or "process-reactive" distinctions. An excessive beta-endorphin response to placebo in schizophrenia is discussed.
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PMID:Response of plasma beta-endorphin immunoreactivity to d-amphetamine and placebo in schizophrenic patients. 629 81


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