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 study of eye movement dysfunction in chronic schizophrenics by electronystagmography revealed a significant increase of saccadic dysmetria as well as saccadic intrusions in smooth pursuit in schizophrenic patients with tardive dyskinesia (TD) compared with those without TD and with healthy controls. The pattern of eye movement dysfunction in schizophrenia allows clear discrimination from patients with similar movement disorders due to Huntington's disease. Of several possible explanation's of the schizophrenic eye movement dysfunction the authors favour the hypothesis of a common pathogenetic link between TD and eye movement disorders in schizophrenia, consisting in an underlying dysfunction of regions involved in the regulation of involuntary attention such as the parietal cortex and striatolimbic structures of the right hemisphere. Recent literature supports the assumption of right hemispheric dysfunction in schizophrenia.
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PMID:Association of tardive dyskinesia with increased frequency of eye movement disturbances in chronic schizophrenic patients. A clinical note. 196 45

1. The tetradecapeptide somatostatin (SS) has a widespread, uneven distribution within several organs including the central nervous system (CNS), with particularly high concentration in the hypothalamus. 2. The SS-related peptides (SS28, SS28(1-12), SS28(15-28)) are originated from the precursor pre-prosomatostatin. 3. SS is suggested to be involved in a large number of CNS functions, locomotion, sedation, excitation, catatonia, body temperature, feeding, nociception, paradoxical sleep, self-stimulation, seizure, learning and memory. 4. SS influences central neurochemical processes. 5. It is possible that SS is related to various neurological and psychiatric illnesses, like Huntington's disease, multiple sclerosis, Parkinson's disease, epilepsy, eating disorders, Alzheimer's disease, schizophrenia and major depressive illness.
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PMID:Preclinical and clinical studies with somatostatin related to the central nervous system. 197 75

Positron-emission tomography (PET), a noninvasive analytical method, made possible the detection of regional alterations in the central nervous system, thus demonstrating "in vivo" the presence of biochemical alterations and the organization of cerebral function in the pathological states. The study of glucose cerebral metabolism velocity, performed recently with the aid of PET, reveals that in the patients with thymic disorders the values recorded for the bipolar syndromes differ from those recorded the for unipolar ones. At the same time, the direct measurement of the activity of the neuroanatomic structures involved in schizophrenia and their response to neuroleptics was possible. This technique and the F-fluoro-desixiglucose method were also applied to the patients with Alzheimer's disease, multi-infarct dementia, Huntington's disease. Wilson's disease and Parkinson's disease. Suggestive alterations of glucose metabolism velocity were noticed and the neuroanatomic structures involved in the pathological manifestations could be specified.
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PMID:[The use of positron-emission tomography in psychiatry]. 198 25

The neuronal dopamine transporter/uptake site can be covalently labeled with the photoaffinity probe 1-(2-[bis-(4-fluorophenyl) methoxy]ethyl)-4-[2-(4-azido-3-[125I]iodophenyl)ethyl]piperazine [( 125I]FAPP) and visualized following sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography. Upon photolysis, [125I]FAPP specifically incorporated into a polypeptide of apparent Mr = 62,000 in membranes from both the putamen and the caudate nucleus of control, Alzheimer's, schizophrenia, and Huntington's diseased brain, and following complete deglycosylation, migrated as an Mr approximately 48,000 polypeptide. In parkinsonian postmortem putamen, however, there was no detectable photoincorporation of [125I]FAPP into the ligand binding subunit of the dopamine transporter. [125I]FAPP did specifically label the Mr 62,000 polypeptide of parkinsonian caudate, although with efficiencies of 20-50% of control. The asymmetrical loss of the dopamine transporter in Parkinson's diseased striatum was confirmed in reversible receptor binding experiments using [3H]GBR-12935 (3H-labeled 1-[2-(diphenylmethoxy) ethyl]-4-(3-phenylpropyl)piperazine). In parkinsonian putamen, mazindol competitively inhibited the binding of [3H]GBR-12935 with an estimated affinity (Ki approximately 2,000 nM) 10 times lower than in controls (Ki approximately 30 nM), while the affinity of maxindol for [3H]GBR-12935 binding in the caudate was equal to that seen with controls (Ki approximately 50 nM). The proportion of [3H]GBR-12935 binding sites recognized by mazindol with high affinity in Parkinson's diseased caudate was, however, reduced by 50-80%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The dopamine transporter is absent in parkinsonian putamen and reduced in the caudate nucleus. 198 18

Matching patients with etiologically distinct but clinically overlapping cognitive disorders on performance of a regionally specific neuropsychological task is a novel and potentially powerful approach to highlighting differences in the pathophysiological mechanisms of impaired cognition. We used this strategy to compare patients with Huntington's disease (HD) and schizophrenia (SC), disorders that share similarities in cognitive impairment. Patients were matched on the basis of performance on the Wisconsin Card Sorting test of "prefrontal" function, after which neuropsychological test data and regional cerebral blood flow data were determined while patients who performed the Wisconsin Card Sorting test were examined. Patients with HD performed worse on visuospatial tasks and recall memory than did patients with SC, although Wechsler Adult Intelligence Scales-Revised IQ and Wechsler Memory Scale memory quotients were equivalent. These differences could not be attributed to differences on the index task, the Wisconsin Card Sorting Test. Patients with HD and SC exhibited a double dissociation in regional cerebral blood flow. The patients with SC had relatively low frontal and high parietal flows, while patients with HD exhibited the reverse of this pattern. Thus, the regional cerebral blood flow and neuropsychological findings in this study appeared to demonstrate that the single final common cognitive impairment of executive function in HD and SC is associated with two markedly dissimilar pathophysiological states.
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PMID:Regional cerebral blood flow and cognitive function in Huntington's disease and schizophrenia. A comparison of patients matched for performance on a prefrontal-type task. 213 83

Synapsin II (formerly known as protein III) is a synaptic vesicle-associated neuronal phosphoprotein that may be involved in the regulation of neurotransmitter release. Synapsin II was studied in postmortem brain samples from 132 individuals with various neuropsychiatric and medical diagnoses. Molecular weight variants of synapsin II were present in 73% of samples from alcoholic individuals but in only 31% of samples from non-diseased individuals, thus confirming our two previous reports of an association between synapsin II variants and alcoholism. The presence of synapsin II variants was not correlated with age or nutritional state. Synapsin II variants were also present in 56% of samples from individuals with schizophrenia and 41% of samples from individuals with Huntington's disease. Synapsin II variants were present in samples from children and young adults, consistent with the possibility that synapsin II variants may reflect a genetically inherited trait. Synapsin II variants were not found in any of 18 rodent models of alcoholism, aging, or vitamin B deficiency, suggesting that synapsin II variants may be a uniquely human trait.
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PMID:An analysis of synapsin II, a neuronal phosphoprotein, in postmortem brain tissue from alcoholic and neuropsychiatrically ill adults and medically ill children and young adults. 214 98

The data on the biochemical mechanisms of the development of neurodestruction are presented. The emphasis is given to glutamate- and aspartate-induced lesions of the brain in hypoxia, hypoglycemia, trauma. The common mechanisms related to secondary hyperfunction of glutamate- and aspartatergic systems underlie the development of chronic neurodegenerative processes in Alzheimer's disease, Huntington's disease, senile dementia, alcoholism, schizophrenia, etc. The basic pharmacological approaches to prevention of destructive processes in the central nervous system are considered.
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PMID:[Endogenous factors of neurodestruction (the pharmacologic aspects)]. 217 97

Evidence from experimental and clinical studies suggests the involvement of the endogenous opioid system in several neurologic and psychiatric disorders (Alzheimer's, Huntington's and Parkinson's diseases, drug-induced movement disorders, Gilles de la Tourette syndrome, stroke, ischemia, brain and spinal cord injury, epilepsy, schizophrenia and affective disorders). However, its involvement is rather a secondary one, perhaps being a severe consequence of a primary, nonopioid disturbance. Thus, treatment of an opioidergic manifestation of a disorder of nonopioidergic origin is necessarily symptomatic and targets only the restoration of the opioid system; such treatment may be beneficial in ameliorating the clinical symptoms of the disorder.
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PMID:The opioid system in neurologic and psychiatric disorders and in their experimental models. 218 70

B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine), a candidate for selective dopamine (DA) autoreceptor agonist activity, was tested for its interactions with biochemical parameters of brain dopaminergic, noradrenergic and serotoninergic systems as measured in ventriculocisternal perfusates of chloralose-anaesthetized cats. DA, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), noradrenaline (NA) and 5-hydroxyindolic acid (5-HIAA) were measured in samples of 30 min collection periods by high-pressure liquid chromatography with electrochemical detection. B-HT 920, in the dose range of 0.03-1 mg/kg i.v., promptly inhibited the efflux of DA and DOPAC in a dose-dependent manner. The 1 mg/kg dose of B-HT 920 reduced the DA levels below 25% of control levels for the whole length of the experiments. The HVA levels were reduced less and in a protracted manner. Only the highest dose of B-HT 920 tested (1 mg/kg) had a significant effect on the level of NA (marked, prompt reduction) and 5-HIAA (delayed, moderate reduction), reflecting its well known alpha 2-adrenoceptor agonist property. The effects of B-HT 920 on the dopaminergic indices were DA receptor-mediated as they were reversed by a low dose (0.05 mg/kg i.v.) of haloperidol. In contrast, the alpha 2-adrenoceptor blocking drug, idazoxan, 4 mg/kg i.v., while it reversed the NA and 5-HIAA reductions did not modify the effect of B-HT 920 on DA, DOPAC and HVA. Thus B-HT 920, in the dose range between 0.03-0.1 mg/kg, selectively affected brain dopaminergic parameters. Our experiments demonstrated that B-HT 920 causes an effective, long lasting and selective suppression of extracellular brain DA levels in vivo. B-HT 920 represents a promising compound for clinical use in pathological conditions known to be ameliorated by a reduction of brain DA activity, such as Huntington's disease, mania and schizophrenia.
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PMID:The dopamine autoreceptor agonist, B-HT 920, preferentially reduces brain dopamine release in vivo: biochemical indices of brain dopamine, noradrenaline and serotonin in ventriculocisternal perfusates in the cat. 246 28

In experiments designed to investigate transmission, cerebrospinal fluid (CSF) from patients with schizophrenia or neurological disease (Huntington's disease) which had been found to induce a cytopathic effect (CPE) in human embryonic fibroblast cell culture was injected intracerebrally into common marmosets. Behavioural observations were made on the animals during a period of 2 1/2 years prior to injection and for 2 1/2 years after injection. In an earlier study (Baker et al. 1983 b) we found that animals injected with CPE + ve CSF became progressively more inactive when compared with those injected with non-cytopathic (CPE -ve) CSF from control patients. In the present study we were unable to replicate this finding. No difference in behaviour emerged between animals injected with control CSF and animals injected with CSF from schizophrenics or patients with neurological disease, nor between animals injected with CPE + ve CSF and animals injected with CPE -ve CSF. The numbers of offspring produced and surviving did not differ between the groups. We conclude that the original findings were due to factors unconnected with the nature of the injected material.
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PMID:A re-investigation of the behavioural effects of intracerebral injection in marmosets of cytopathic cerebrospinal fluid from patients with schizophrenia or neurological disease. 250 49


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