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)

Enzymes concerned with neurotransmitter metabolism were measured postmortem in 50 regions from the brains of 11 chronic schizophrenics, 2 patients with senile dementia, 1 depressive, and 18 controls. Enzymes studied were tyrosine hydroxylase, dopa decarboxylase, glutamic decarboxylase, choline acetyltransferase (CAT), and acetylcholinesterase. The schizophrenic group had high CAT activities in the hippocampus, caudate, putamen, and nucleus accumbens; the other patients from the same hospital did not. A compensatory response to long- or short-term drug usage is considered, but correlations are hard to establish in the group studied. An alternative hypothesis proposes that the high levels are a compensatory response to defective cholinergic receptors in the affected areas. On this hypothesis, and by analogy with chorea, dopaminergic antagonists would act in schizophrenia by helping to reestablish cholinergic-dopaminergic balance.
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PMID:Possible changes in striatal and limbic cholinergic systems in schizophrenia. 4 82

Comparison of the properties of blood platelets and serotonergic synaptosomes suggests that the human platelet can serve as an appropriate model for the transport, metabolism, and release of serotonin (5-HT) by CNS serotonergic neurons. The study of blood 5-HT levels and platelet 5-HT pharmacodynamics in patients with a variety of psychiatric and neurologic disorders has generated interesting leads into possible abnormalities of CNS 5-HT neurons in these patients. This article reviews the experimental evidence, which uses the human platelet model to investigate neurotransmitter-related abnormalities in Down syndrome, mental retardation, infantile autism, hyperactivity syndromes (minimal brain dysfunction), schizophrenia, affective disorders, Duchenne muscular dystrophy, Parkinson disease, Huntington chorea, and migraine headaches.
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PMID:The human platelet. A diagnostic and research tool for the study of biogenic amines in psychiatric and neurologic disorders. 14 Jun 32

One of the earliest Nazi efforts to create a super race was the mass sterilization of German citizens through radiation or surgery. A law enacted on July 14, 1933 stated that all patients suffering from hereditary mental disorders, schizophrenia, manic-depressive psychosis, hereditary epilepsy, chorea, blindness, deafness, other serious hereditary defects or alcoholism must be sterilized. Special courts were created. Directors of psychiatric institutions, certain doctors, as well as the patients themselves were called before the court. All medical personnel including nurses and midwives were to report anyone in their care who should be sterilized. Patients had the alternation of willingly committing themselves for life into a "closed" institution, where they would have no opportunity for heterosexual actifity. On the whole, German society did not support this law, particularly relatives and family of patients. From the sketchy records available, it is clear that there were often casualties and that patients were hunted out and forced to submit to sterilization.
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PMID:[Compulsory sterilization in the Breslau district in 1934-1944]. 37 15

There are some evidences to propose blood platelets as a model of bioaminergic neurons. Similarities between platelets and neurons are particularly important with respect to serotonin metabolism but now it is possible to extend this model to other neurotransmitters such as dopamine, GABA, glutamate... The reason for these similarities may be due to the common embryonic origin of these two very different cell types. Some changes of platelet functions are observed in psychiatric syndromes. For example: serotonin uptake, bioamine storage, enzymatic activities are modified in different types of depression and schizophrenia, infantile autism, neurologic diseases (migraine, chorea, Down syndrom). Furthermore, psychotropic drugs also alter the platelet functions. Recently, the discovery of neuro-endocrine disorders in psychiatric diseases has led to the proposal of platelets as a model in neuro-endocrinology. Some arguments can be developed to support this hypothesis. In biological psychiatry, the platelet model seems actually useful essentially in the classification of psychiatric diseases, the management of treatments and the study of new psychotropic drugs. However methodologic difficulties still presently limit the development of this model.
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PMID:[Blood platelets: neuronal model in psychiatric disorders]. 286 6

The marked variability of psychiatric and neurological features of Huntington's chorea is described in a large family consisting of 31 members of two filial generations and the parenteral generation, of which 13 members showed manifest signs of the disease, while two further members died probably in a preliminary stage of the disease. It is of interest that a few members of the family had a large number of children, while the majority remained without offspring. Analysis of the psychiatric symptoms and signs shows that the course of the disease may take either a quiet demential, or a turbulent form. In the latter the features of manic-depressive psychosis or of schizophrenia occur, as well as a syndrome resembling psychopathic states with explosive-violent features comparable to the pseudo-psychopathia syndrome of U. H. Peters. The quiet demential course is correlated to progressive cerebral atrophy. The different forms of the turbulent course may be due to additional, genetically determined radicals of both groups of psychoses, to localized differences in the progression of the cerebral atrophy or to unspecific noxious influences from the external or internal milieu. With regard to neurological features, apart from the signs of chorea, akinesic rigidity and tic-like hyperkinesias with transition into stereotypes and primitive motor patterns were observed, as well as an apallic syndrome in the terminal phase. As a rare psychiatric variant, a syndrome characterized by compulsive pedantry combined with tic-like hyperkinesias was observed. The possibility of a striatal lesion causing motor and psychiatric impulsive features is pointed out.
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PMID:[Phenomenology of Huntington chorea, analysis of a large family]. 316 Jan 72

In experiments designed to investigate transmission, cerebrospinal fluid (CSF) from patients with schizophrenia and neurological disease (huntington's chorea and multiple sclerosis) which had been found to induce cytopathic effects in human embryonic fibroblast cell culture was injected intracerebrally into mice, hamsters and marmosets (small New World primates). No evidence was obtained of transmission to mice or hamsters. A total of 15 marmosets (Callithrix jacchus) was injected intracerebrally with CSF [8 with samples from 4 patients with schizophrenia. 3 with samples from patients with neurological disease (2 with Huntington's chorea and 1 with multiple sclerosis) and 4 with samples from 3 patients without neurological or psychiatric disease] and was observed over a period of 2 1/2 years. Analysis of variance on data obtained from behavioral observations averaged over 6-month periods revealed that animals injected with CSF from patients with schizophrenia and neurological disease became progressively more inactive when compared with animals injected with CSF from control patients. The change detected by behavioural observation was confirmed as a difference 2 and 2 1/2 years after injection by automated activity monitoring. There was an incidence of reproductive anomalies (including two occipital encephalocoeles) in the females in the experimental group, but the numbers are too small to draw firm conclusions from this observation. Many reported differences in biological samples from schizophrenic patients and normal controls have subsequently been found to be due to factors unrelated to the disease state. This may prove to be the case with the changes observed in this experiment. Nevertheless, the fact that marmosets injected with CSF from patients suffering from neuropsychiatric disease, including schizophrenia, subsequently differed in their behaviour from those injected with control CSF warrants further investigation.
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PMID:An investigation of the effects of intracerebral injection in the marmoset of cytopathic cerebrospinal fluid from patients with schizophrenia or neurological disease. 622 54

The psychiatric manifestations of Huntington's Disease (HD) include dementia, irritability and apathy, a major affective syndrome, and hallucinosis. The theoretical and practical utility of chorea as a focus of research interest in HD is questioned, whereas the data reviewed suggest that assessments of cognition, functional capacity and motor impairment are better correlated neuropathologically, and are better indicators of disease severity and progress than chorea. The high incidence of major affective disorders on modified DSM III criteria among HD patients (41 per cent) may be explained either as a manifestation of genetic heterogeneity within the HD phenotype or on the basis of genetic linkage between HD and manic depressive illness (MDI). This is supported by the high coincidence of HD and MDI (20 out of 23) among secondary cases of HD ascertained through probands having both disorders, indicating a strong familial clustering of the association. This implies that a young adult at risk for HD who has had episodes of severe depression has considerably more than 50 per cent likelihood of progressing to manifest HD. Although auditory hallucinations appear occasionally in patients with HD, most do not meet current criteria for schizophrenia.
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PMID:Psychiatric features of Huntington's disease: recent approaches and findings. 623 7

A rare disorder, neuroacanthocytosis is characterized by chorea, tics, subcortical cognitive impairments, and acanthocytosis. This study presents two men with neuroacanthocytosis who were initially diagnosed with schizophrenia. Findings revealed the intricate relationships between movement disorders and psychosis and the importance of accurate diagnoses.
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PMID:Schizophrenia-like presentation of neuroacanthocytosis. 1292 18

Causes and pathogenesis of psychiatric disorders is poorly understood. Infections by viruses or other agents may disturb neurotransmitters and elicit behavioral abnormalities, and induce long lasting immune reactions, referred to as mild encephalitis (ME). New findings (pathology, biochemistry, imaging) in schizophrenia and bipolar psychoses are compatible with ME hypothesis. In Chorea Sydenham and PANDAS syndrome autoimmune ME seems to explain anxiety-compulsive-hyperactivity symptoms. Add-on-therapy with Cox-II-blockers or valacyclovir improved acute schizophrenia, CSF filtration some cases of therapy resistant psychoses.
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PMID:[The mild encephalitis-hypothesis--new findings and studies]. 1557 Apr 97

Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.
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PMID:Neurologic presentation of celiac disease. 1582 33


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