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)

Dopamine receptor types D1 and D2 can oppose or enhance each other's actions for electrical, biochemical, and psychomotor effects. We report a D1-D2 interaction in homogenized tissue as revealed by ligand binding. D2 agonists lowered the binding of [3H]raclopride to D2 receptors in striatal and anterior pituitary tissues. Pretreating the tissue with the D1-selective antagonist SCH 23390 prevented the agonist-induced decrease in [3H]raclopride binding to D2 sites in the striatum but not in the anterior pituitary, which has no D1 receptors. Conversely, a dopamine-induced reduction in the binding of [3H]SCH 23390 to D1 receptors could be prevented by the D2-selective antagonist eticlopride. Receptor photolabeling experiments confirmed both these D1-D2 interactions. The blocking effect by SCH 23390 was similar to that produced by a nonhydrolyzable guanine nucleotide analogue, and SCH 23390 reduced the number of agonist-labeled D2 receptors in the high-affinity state. Thus, the D1-D2 link may be mediated by guanine nucleotide-binding protein components. The link may underlie D1-D2 interactions influencing behavior, since the link was missing in over half the postmortem striata from patients with schizophrenia and Huntington disease (both diseases that show some hyperdopamine signs) but was present in human control, Alzheimer, and Parkinson striata.
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PMID:Link between D1 and D2 dopamine receptors is reduced in schizophrenia and Huntington diseased brain. 257 62

Past studies on the occurrence of atypical lymphocytes in the blood of individuals with schizophrenia are contradictory; some researchers have argued that such cells are a genetic marker of the disease while others have explained the cells simply as an effect of antipsychotic drugs. The present study blindly measured atypical lymphocytes in 14 schizophrenics on medication for at least 6 weeks and off medication for at least 4 weeks, ten Huntington's disease patients on antipsychotic medication, and ten normal controls. The patients with schizophrenia (P less than 0.05) and those with Huntington's disease (P less than 0.02) both had significantly more atypical lymphocytes than the normal controls. However no difference was found in the percentage of atypical lymphocytes in patients with schizophrenia on and off medication. The authors cite the need for studies of first-admission, never-tested patients to definitively settle this question.
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PMID:Medication effect on lymphocyte morphology in schizophrenia. 257 75

Family, twin, and adoption studies have suggested an important role for hereditary factors in the etiology and pathogenesis of several psychiatric disorders. Advances in molecular and statistical genetics may very well reveal the identity of these factors, which may include single genes. Linked markers, critical to the discovery of abnormal genes in several medical conditions, have been reported for Huntington's disease, Alzheimer's disease, bipolar disorder, and schizophrenia. Psychiatric disorders pose particular problems (etiologic heterogeneity, incomplete penetrance, variable expressivity) for genetic research. New practical and ethical questions also arise. Nevertheless, knowledge may emerge that will suggest new approaches to diagnosis, prevention, and treatment.
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PMID:Genetics and psychiatry: past discoveries, current dilemmas, and future directions. 281 38

Since 1982, grafting of human nervous tissue on human central nervous system has been realized, mainly in Parkinson's disease. The present article reviews the theoretical basis of such procedures, i.e., the remarkable experimental work that began around the turn of the century. New approaches, e.g., using hydroxydopamine or MTPP, have greatly enlarged the field of experimental research. In man, grafts of adrenal medulla and, in a few cases, of fetal substantia nigra, have been realized in several hundreds of patients. The known results invite great caution. Brain grafting has also been considered in Huntington's chorea, trauma of the spinal cord and even schizophrenia. In animals, transplants of hypothalamus and pre-optic area have counteracted genetic endocrine disorders. Experimental researches are of high interest but their application to man raises major problems of efficiency and fundamental ethical and legal questions.
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PMID:[Homografts in the human brain. Current data]. 267 72

Positron emission tomography (PET) is emerging as a very useful clinical tool and is adding a great deal to our understanding of the pathophysiology of central nervous system (CNS) disorders. Although computed tomography (CT) and magnetic resonance imaging (MRI) have had a dramatic impact on patient management, there is often an important associated function abnormality which is best assessed by PET. In normal aging and in dementia, the CT and MRI brain changes of atrophy and white matter abnormalities are frequently nonspecific. PET has been more diagnostic, showing characteristic regional metabolic abnormalities. Evaluation of brain tumors such as astrocytomas with PET has demonstrated better correlation with histologic grade compared to CT. Unlike CT or MRI, PET can help to distinguish radiation necrosis from recurrent tumor, and can differentiate the extent of metabolically active tumor from surrounding edema. PET is useful in evaluating stroke patients, providing better prognostic information and demonstrating abnormalities sooner than CT. In epilepsy, PET appears to be superior to MRI in localizing seizure foci in patients with partial seizures. In head trauma patients, metabolic patterns are being described which will likely have an effect on patient management. The use of PET in schizophrenia has yielded very interesting results, with common patterns of metabolic abnormalities being demonstrated. CT and MRI in these patients have not been very useful. PET has also shown promise in movement disorders such as Huntington's disease. It is now clear that PET is already clinically useful and can provide valuable information unobtainable by CT and MRI. As new radioligands are developed, PET is certain to assume an even more important role in the future.
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PMID:PET, CT, and MRI in the evaluation of neuropsychiatric disorders: current applications. 267 65

Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement of concentration and attention span. Nicotine gum alone was without effect. While 80% of children showed improvement with nicotine gum, 70% completely discontinued the gum because of side-effects, primarily involving nausea and bitter taste. Nicotine may prove useful for treating other neuroleptic responsive disorders, such as schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome. 273 Sep 49

Using highly sensitive nucleic acids hybridization techniques, which allow the detection of 0.1-0.5 single copy gene equivalents per cell, DNA from the temporal cortex of seven definite schizophrenics, five persons with schizophrenia-like psychoses, three patients with Huntington's chorea and nine mentally normal individuals were probed with human cytomegalovirus (HCMV) DNA. A clear hybridization signal was obtained with DNA from the temporal lobe of a young schizophrenic patient, whereas DNA from the temporal cortex of controls did not hybridize to the HCMV probe. This finding is in agreement with the cytomegalovirus hypothesis of schizophrenia and hints at the possibility that viral infection of the temporal cortex may in some sporadic cases be a contributing factor to the development of schizophrenic psychoses. There is no indication, however, that infection of the central nervous system with HCMV is an aetiological factor in the great majority of schizophrenic disorders. Clearly further studies, preferably in situ hybridizations of whole brains, are needed to prove or disprove the cytomegalovirus hypothesis of schizophrenia.
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PMID:Human cytomegalovirus DNA in the temporal cortex of a schizophrenic patient. 285 Jan 88

Studies describing the CNS distribution of neuropeptides can provide important new insights concerning their possible physiological functions. The rational for studying human post-mortem tissue, as well as some methodological constraints, are reviewed. The localization of NT in normal human brain is presented. Concentrations of NT, TRH, and SRIF were determined in brain tissue from normal controls and patients with schizophrenia or Huntington's chorea. Specific alterations in the levels of these neuropeptides were found in each disease. Appreciable quantities of NT immunoreactivity are present in human CSF. Sub-normal CSF-NT levels were found in a sub-group of unmedicated schizophrenics but were elevated back to normal concentrations following neuroleptic treatment. Although the pathophysiological significance of these findings is unclear, they nevertheless indicate that neuropeptides are important brain constituents which deserve further study.
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PMID:Neuropeptides in CSF and post-mortem brain tissue of normal controls, schizophrenics and Huntington's choreics. 285 37

In anesthetized cats the dopamine autoreceptor agonist B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine), 1 mg/kg i.v., greatly decreased the amount of dopamine in cerebroventricular perfusates. This effect was antagonized by a low dose (50 micrograms/kg i.v.) of haloperidol, but not by the alpha 2-adrenoceptor blocker idazoxan. Our observations provide evidence that B-HT 920 inhibits brain dopamine release in vivo and may be therapeutically valuable in diseases presumed to be accompanied by a predominance of brain dopamine activity, such as Huntington's disease, mania and schizophrenia.
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PMID:The dopamine autoreceptor agonist B-HT 920 inhibits in vivo dopamine release into the cerebroventricular system of cats. 288 21

Somatostatin was originally isolated as a 14-amino-acid peptide from the ovine hypothalamus. The peptide has a widespread regional distribution within the central and peripheral nervous systems, as well as in peripheral organs. Preservation of the chemical structure over a wide range of vertebral species indicates important functional roles of the peptide. Recent results about the role of somatostatin and related peptides in different psychiatric (depression, schizophrenia, Alzheimer's disease) and neurological (Huntington's disease, multiple sclerosis, Parkinson's disease) diseases, and the effects on the hypothalamic-pituitary-adrenal axis are summarized. Also, the influence of some psychotropic drugs (halo-peridol, carbamazepine) on somatostatin levels in cerebrospinal fluid is discussed.
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PMID:Brain and CSF somatostatin concentrations in patients with psychiatric or neurological illness. An overview. 290 14


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