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)

In 36 drug-free schizophrenic patients, lumbar CSF was analyzed by mass fragmentography for the major monoaminergic transmitter metabolites 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG). High or deviant concentrations of 5-HIAA were significantly related to a family history of schizophrenia. For patients with deviant 5-HIAA levels, the probability for a family history of schizophrenia was eight times higher than in subjects with normal values. High concentrations of HVA also tended to be significantly related to a family history of schizoprenia. The majority of schizophrenic patients, who lacked family history for the disorder, had normal monoamine metabolite concentrations in CSF. The results suggest a coupling between biochemical variables related to central serotonin and dopamine metabolism and forms of schizophrenia that have a familial disposition.
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PMID:Aberrant monoamine metabolite levels in CSF and family history of schizophrenia. Their relationships in schizophrenic patients. 615 28

Antibrain antibody titers were determined by hemagglutination technique in sera and cerebrospinal fluid of 54 schizophrenic patients and 27 nonschizophrenic controls. Antibrain antibodies were detected in sera and CSF of 26 (48.1%) schizophrenics but in none of the controls. They were significantly more often present in those schizophrenics who had a past history (p less than 0.01) and family history (p less than 0.01) of schizophrenia. They had no significant relationship with the subtype and the duration of schizophrenia. The possible genetic and immunological implications of these findings are discussed.
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PMID:Autoimmune model of schizophrenia with special reference to antibrain antibodies. 618 98

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured in the spinal fluid of 45 women hospitalized in a psychiatric department for major depression (14 cases), schizophrenia (18 cases) and alcohol dependence (13 cases). Dexamethasone suppression tests were performed following CSF examinations in all patients, and TRH stimulation tests were also made in six subjects. All biological examinations were carried out in a drug-free state. The Marke-Nyman Temperament scale was administered to all patients as soon as severe psychotic disturbances subsided and sufficient cooperation was achieved, but no later than 10 days following biological examinations. The MNT was repeated after recovery to check reliability of the test results during an episode of a psychiatric disorder. CSF amine metabolite concentrations did not differ significantly in the three patient groups; postdexamethasone average cortisol levels were above the critical level (5 micrograms/dl) in each group, the highest values being found in major depression. One of the three MNT factors was inhomogeneous among diagnostic groups (validity: low in depression and alcoholism), but the other two also differed from a healthy control population. Correlation structure between biological and psychological variables was homogeneous throughout the diagnoses and a significant inverse correlation was found only between CSF 5-HIAA and the validity factor of MNT. Maximal TSH response to TRH stimulation correlated with both solidity and stability in the MNT scale. Since MNT results proved to be stable even during an illness episode, a possible link is suggested between personality traits and central serotonin metabolism.
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PMID:Relationship between cerebrospinal fluid amine metabolites, neuroendocrine findings and personality dimensions (Marke-Nyman scale factors) in psychiatric patients. 619 Mar 56

The effect of 1 mg dexamethasone on CSF levels of 5-hydroxyindoleacetic acid (5 HIAA), homovanillic acid (HVA) and cortisol (CS) was investigated in 100 psychiatric inpatients: 45 subjects had their lumbar punctures 1-4 days following dexamethasone administration, and the results were compared with those from 55 other patients investigated before drug ingestion. All patients were women, and none had received psychotropic medication for at least two weeks before the study. Seven subjects consented to two LPs both before and after dexamethasone. As expected, cortisol in the CSF significantly decreased after dexamethasone: the decrease was greatest 10 hours following the drug. HVA showed a weak and transient elevation after 10 hours only. CSF 5 HIAA was found to be significantly increased in postdexamethasone samples and high levels were still found even after 82 hours. Diagnostic differences (major or minor depression, schizophrenia, alcohol abuse or dependence) did not account for the observed differences. Repeated CSF examinations in seven subjects corroborated these findings: all cortisol values were decreased and all 5 HIAA values were increased after dexamethasone while HVA values showed random changes. The data may suggest that serotonergic mechanisms may be involved in dexamethasone action in the CNS. In addition, dexamethasone administration can alter CSF 5 HIAA level, a possible factor which should be taken into consideration in CSF studies.
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PMID:The effect of dexamethasone on cerebrospinal fluid monoamine metabolites and cortisol in psychiatric patients. 619 44

One hundred and ten patients with Research Diagnostic Criteria (RDC) diagnoses of major depressive disorders were assessed for present or recent suicidal ideation and behavior and for suicidal acts earlier in life before current depression using the Schedule for Affective Disorders and Schizophrenia (SADS). Suicidal scores were correlated uni- and bivariately with levels of CSF monoamine metabolites (HVA, 5HIAA, MHPG), urinary MHPG, the proportion post-/predexamethasone plasma cortisol at 1100 h, and platelet MAO activity (all standardized to same sex, age, height and weight). Results indicate that all 3 monoamine metabolites and their interactions are involved in various aspects of suicidality, at least in unipolar patients. MHPG and 5HIAA (both low or both high) were involved in current or recent suicidal ideation, and low HVA was mainly associated with past potential lethality of suicidal acts. Current hypercortisolism was found in patients that earlier in life had tried to commit dangerous suicides. Bipolar patients (depressives with a history of manic or hypomanic episodes) had earlier in life significantly more, and more dangerous, suicidal attempts than the unipolars.
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PMID:Life at risk: markers of suicidality in depression. 620 42

Using a radioimmunoassay procedure substance P-like activity was measured in samples of human CSF obtained from 12 patients with major depressive disorder, 12 with schizophrenia, and 15 control cases diagnosed as psychiatrically normal. Levels were significantly higher in CSF of patients with depressive disorder as compared with schizophrenic patients or controls. Chemical characterization revealed that the measured activity was less basic than substance P itself and might be due to C-terminal fragments. A component reacting with an antiserum highly specific for the substance P[1-7]fragment was found in CSF of patients with depressive disorder. The results indicate that substance P-related peptides may be biological markers in psychoses, particularly in major depressive disorder.
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PMID:Elevation of substance P-like peptides in the CSF of psychiatric patients. 620 62

Tissue cultures were inoculated with CSF from patients with schizophrenia and some other psychiatric and neurological illnesses. The CPE was readily seen in all 13 strains of human skin fibroblasts examined but could not be serially passaged. The results of retesting many specimens, either by the same worker or under full double blind conditions, usually agreed and thus indicate that the CPE was due to the CSF and not to non specific changes in the cultures. CPE was seen in cultures in which mycoplasmas could not be detected. Degenerated cultures show polymorphous nuclei with condensed nuclear chromatin and enlarged mitochondria with few cristae but virus particles were not identified. The physical properties of the agent in the CSF that induced the CPE were the same as those reported earlier for CSF from schizophrenic patients.
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PMID:Further studies of the cytopathic effect in tissue cultures inoculated with CSF from patients with schizophrenia and other nervous system diseases. 622 51

Recent studies have found elevated levels of norepinephrine (NE) in CSF and brain specimens from schizophrenic patients. Presynaptic inhibitory alpha 2-adrenergic receptors regulate NE release in the brain. The hypothesis that the functional sensitivity of this presynaptic regulation of NE is impaired in schizophrenia was tested by evaluating, in schizophrenic patients and age-matched normal controls, the ability of clonidine, an alpha 2 agonist, to lower plasma levels of the NE metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and to lower blood pressure (BP). Clonidine produced a significant decrease in plasma MHPG levels in the normal control group, but did not lower plasma MHPG levels in the schizophrenic patients. Clonidine decreased BP equally in both groups. These results suggest that there is a functional subsensitivity of the inhibitory presynaptic alpha 2-adrenergic receptor in schizophrenia, which may relate to an impaired regulation of NE turnover.
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PMID:Impaired presynaptic regulation of norepinephrine in schizophrenia. Effects of clonidine in schizophrenic patients and normal controls. 627 49

In this paper we have reported the results of studies in psychiatric patient groups using the strategy of measuring opioid activity and beta-endorphin (ir) in CSF. Our findings do not lend support to the notion of excess endorphin activity in schizophrenia, but rather suggest the possibility of a decrease in endogenous opioid activity in some schizophrenic patients. In affectively ill patients our data suggest that there may be a relative change in endogenous opioid system activity across state change in manic-depressive illness. Who also found a relationship between nurses' ratings of anxiety and CSF opioid activity in depressed patients, although it is unknown whether this directly relates to the pathophysiology of this symptom, or is related to stress response. The relationship between CSF opioid activity and HPA axis activity, as reflected by urinary free cortisol excretion, supports the notion of important physiologic relationships between these systems and raises the issue of a role for the endogenous opioid system in the abnormal activation of this system in depression. Finally, the finding of increased CSF opioid activity in anorexia nervosa patients when a minimum weight coupled with data relating endogenous opioids to eating behavior raises interesting questions regarding a possible involvement of the endogenous opioid system involvement in this illness.
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PMID:Endorphins in the cerebrospinal fluid of psychiatric patients. 629 60

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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