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)

A retrospective chart review of 50 pharmacotherapeutically resistant patients was performed after treatment with NET in 1986-1988. 28 patients suffered from schizophrenia and 22 from affective psychosis. In contrast to literature where NET as therapy of first choice has favourable results in depression in this study 60.7% of the treatment resistant acute schizophrenics responded well to NET. 3 months after discharge from hospital 9 schizophrenics (32.1%) but only 3 patients with affective psychosis (13.6%) presented a 'good' outcome (full remission). A longer duration of schizophrenia (more than 5 years since first manifestation) and a good response to neuroleptics in history was predictive for a good actual NET response (14 of 17 patients), whereas 7 of 11 patients suffering from schizophrenia less than 3 years without any period of full remission on neuroleptics were also non-responders to NET.
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PMID:[Effectiveness of neuro-electric therapy in drug resistant endogenous psychoses]. 167 54

The presence of high concentrations of both dopamine and cholecystokinin (CCK) in the striatum and in various limbic structures suggests that the CCK may not only influence dopaminergic transmission, but it also may be relevant to the psychopathology of schizophrenia and to the therapeutic effects of neuroleptics. By using a synaptosomal fraction isolated from the mouse cerebral cortex and [propionyl-3H]CCK8-sulphate ([3H]CCK8S) as a ligand, a single binding site for [3H]CCK8 with a KD value of 1.04 nM and a Bmax value of 42.9 fmol/mg protein was identified. The competitive inhibition of [3H]CCK8S binding by related peptides produced an order of potency of CCK8-sulphated (IC50 = 5.4 nM) greater than CCK8-unsulfated (IC50 = 40 nM) and greater than CCK4 (IC50 = 125 nM). The regional distribution of [3H]CCK8S binding in the mouse brain was highest in the olfactory bulb (34.3 +/- 5.6 fmol/mg protein) greater than cerebral cortex greater than cerebellum greater than olfactory tubercle greater than striatum greater than pons-medulla greater than mid brain greater than hippocampus greater than hypothalamus (12.4 +/- 2.1 fmol/mg protein). The repeated administration of haloperidol (2.5 mg/kg/tid) increased the binding of [3H]CCK8S in cerebral cortex from 31.8 +/- 1.7 to 38.9 +/- 5.2 fmol/mg protein. The varied distribution of CCK8S receptors may signify nonuniform functions for the octapeptide in the brain.
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PMID:Characterization of [3H]cholecystokinin octapeptide binding to mouse brain synaptosomes: effects of neuroleptics. 362 61

Using a quantitative RNA-PCR approach tyrosine kinase receptor (trk) C mRNA levels were determined in brain material from the frontal cortex (BA10), temporal cortex (BA20) and cerebellum of control specimen and patients with schizophrenia, bipolar disorder or non-psychotic depression (15 subjects each). In the frontal cortex of schizophrenics there was a 5.8-fold reduction of trk C mRNA levels, which reached statistical significance (P < 0.05). Trk C levels in the cerebellum were positively correlated with lifetime fluphenazine equivalents (r = 0.54), suggesting that neuroleptics influence TRK C gene activity in the cerebellum. Moreover, the distinct medication-independent reduction of trk C mRNA may point to a disturbed neurotrophic gene activity in the frontal cortex of schizophrenic patients.
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PMID:Reduced tyrosine kinase receptor C mRNA levels in the frontal cortex of patients with schizophrenia. 986 28

Estimates of the direct costs of mental health services for patients with schizophrenia are made from a registration of all patients seen during a period of 4 weeks in all treatment units serving 6 catchment areas. The estimates were based on unit costs. The total direct costs of mental health services for schizophrenic patients in Norway were estimated to be NOK 1158 million (US$ 164 million). In total, 74.3% of the costs are for long-term in-patient care, 19.7% are for acute and intermediate length in-patient care, and 6.0% are for out-patient and day care. The average costs of schizophrenic patients with a GAF score of 1-20 are almost twice those of patients with a GAF score of 21-40, and more than three times those of patients with a GAF score of 41-60.
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PMID:Costs of services for schizophrenic patients in Norway. 1008 87

The Chromosome 5 Workshop heard new data on a schizophrenia susceptibility locus in the 5q23.3-q31.1 region. Sixty-two pedigrees from Finland gave a lod score of 1.36 at the CSF1R locus approximately 14 cM distal to IL9/D5S393, where positive results from three pedigree collections converged at the 1997 workshop. Though positive at CSF1R, the new data were only weakly positive at the IL9 (lod 0.46) and D5S393 (lod 0.07) loci themselves. The workshop also reviewed new evidence in the 5p14.1-p13.1 region, where a large pedigree of schizophrenia of Puerto Rican extraction has suggested a susceptibility locus with a maximum lod score at D5S111. Twenty-one new pedigrees multiplex for schizophrenia in African Americans gave positive lod scores at D5S111 and flanking loci. In bipolar illness five genetically related pedigrees from the Saguenay-Lac-St. Jean region of Quebec identified a region of interest at 5q31.3-q35.1. This region overlaps with the D5S423 locus and includes the D5S812 locus and the 5q34 region, all of which are consistent with linkage in at least one other study.
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PMID:Report of the Chromosome 5 Workshop of the Sixth World Congress on Psychiatric Genetics. 1037 36

Hare's Psychopathy Checklist--Revised (PCL-R) was used to test the hypothesis that psychopathy predicts violent recidivism in a cohort subjected to forensic psychiatric investigation and consisting of male violent offenders with schizophrenia (N = 202). Psychopathy was assessed with retrospective file-based ratings. Mean follow-up time after detainment was 51 months. Twenty-two percent of the offenders had a PCL-R score > or = 26 (cutoff), and the base rate for violent recidivism (reconvictions) during follow-up was 21%. Survival analysis revealed that psychopathy was strongly associated to violent recidivism (log-rank = 17.71, df = 1, p < 0.0001). The area under the curve (AUC) of the receiver operating characteristics (ROC) of PCL-R total score to predict violent recidivism varied between different time frames from .64 to .75. Cox regression analyses revealed that other potential risk factors could not equally well or better explain violent recidivism in the cohort than psychopathy as measured by PCL-R.
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PMID:Psychopathy (PCL-R) as a predictor of violent recidivism among criminal offenders with schizophrenia. 1069 18

This study explored characteristic subjective experiences of schizophrenia. A questionnaire for self-assessment of disturbances in several cognitive and perceptual areas (the Eppendorf Schizophrenia Inventory, or ESI) was constructed and administered to first-episode schizophrenics (SCHe, n = 45), negative syndrome schizophrenics (SCHn, n = 45), remitted schizophrenics (SCHr, n = 24), depressives (DEP, n = 43), alcoholics (ALK, n = 48), obsessive-compulsive patients (ZWA, n = 46), and healthy controls (KON, n = 57). Comparisons between the SCHe, SCHn, DEP, ALK, and ZWA groups and a subsequent factor analysis revealed four schizophrenia-specific dimensions: attention and speech impairment (AS), ideas of reference (IR), auditory uncertainty (AU), and deviant perception (DP). Further analyses suggested that the AS syndrome may represent a mediating vulnerability factor while IR, AU, and DP probably are reversible episode indicators. The results may contribute to refinements in the measurement of specific prepsychotic signs, thus facilitating the development of early intervention approaches.
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PMID:[The Eppendorf Schizophrenia Inventory (ESI). Development and evaluation of a questionnaire for assessment of characteristic self perception of cognitive dysfunctions by schizophrenic patients]. 1110 63

Biogenic amine transporters, namely the dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (serotonin, 5-HT) transporters (DAT, NET and 5-HTT, respectively) appear to be the key elements in regulating biogenic amine neurotransmission. These proteins therefore represent a primary target for therapeutic intervention in the treatment of numerous psychiatric disorders, such as depression, anxiety and perhaps even schizophrenia as well as drug abuse. The cloning of DAT, NET and 5-HTT and development of selective radioligands for them over the last decade has dramatically increased our understanding of their location, structure and function. These breakthroughs have also enabled remarkable progress in determining how biogenic amine transporters are regulated under not only normal conditions but also when confronted with acute or chronic exposure to a variety of stimuli including psychotherapeutic drugs. Because of the important therapeutic consequences of a better understanding of these transporters, the present review discusses recent advances in defining their mechanism of action, location and regulation and the implications of the newer data for neuropsychopharmacology.
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PMID:New views of biogenic amine transporter function: implications for neuropsychopharmacology. 1128 47

Altered dopamine regulation in the medial prefrontal cortex has been linked to drug abuse and disorders such as schizophrenia. Heterogeneous expression of the dopamine transporter, as well as the ability of the norepinephrine transporter to clear dopamine in the prefrontal cortex, delineates two potential sites for the regulation of synaptic dopamine within the cortex. The present study used in vivo microdialysis to compare the effects of local infusions of dopamine and norepinephrine uptake blockers in the caudate putamen and two subregions of the prefrontal cortex, the anterior cingulate and prelimbic/infralimbic cortices. Results revealed that all dopamine uptake blockers produced greater increases in dopamine efflux in the caudate-putamen relative to the prefrontal cortex. In addition, amphetamine administration increased dopamine efflux to a greater degree in the prelimbic, relative to the anterior cingulate, cortex. In contrast, the increase in dopamine efflux was similar in both subregions in the presence of nomifensine and desmethylimipramine. Infusions of the selective dopamine uptake blocker GBR 12909 failed to alter dopamine efflux in any prefrontocortical subregion. These data indicate a more prominent role for the dopamine transporter in the clearance of extracellular dopamine in the caudate-putamen relative to the prefrontal cortex and an important role for NET in the clearance of dopamine in both the prelimbic and anterior cingulate subregions of the rat medial prefrontal cortex.
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PMID:Effects of catecholamine uptake blockers in the caudate-putamen and subregions of the medial prefrontal cortex of the rat. 1198 30

The common fragile site FRA6F, located at 6q21, is an extended region of about 1200 kb, with two hot spots of breakage each spanning about 200 kb. Transcription mapping of the FRA6F region identified 19 known genes, 10 within the FRA6F interval and nine in a proximal or distal position. The nucleotide sequence of FRA6F is rich in repetitive elements (LINE1 and LINE2, Alu, MIR, MER and endogenous retroviral sequences) as well as in matrix attachment regions (MARs), and shows several DNA segments with increased helix flexibility. We found that tight clusters of stem-loop structures were localized exclusively in the two regions with greater frequency of breakage. Chromosomal instability at FRA6F probably depends on a complex interaction of different factors, involving regions of greater DNA flexibility and MARs. We propose an additional mechanism of fragility at FRA6F, based on stem-loop structures which may cause delay or arrest in DNA replication. A senescence gene likely maps within FRA6F, as suggested by detection of deletion and translocation breakpoints involving this fragile site in immortal human-mouse cell hybrids and in SV40-immortalized human fibroblasts containing a human chromosome 6 deleted at q21. Deletion breakpoints within FRA6F are common in several types of human leukemias and solid tumors, suggesting the presence of a tumor suppressor gene in the region. Moreover, a gene associated to hereditary schizophrenia maps within FRA6F. Therefore, FRA6F may represent a landmark for the identification and cloning of genes involved in senescence, leukemia, cancer and schizophrenia.
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PMID:Cloning and characterization of the common fragile site FRA6F harboring a replicative senescence gene and frequently deleted in human tumors. 1237 Aug 18


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