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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential importance of vasospasm, with or without consequent thrombosis, as a mechanism in general disease is discussed and the evidence examined in one organ, namely the brain. It is concluded that vasospasm might be important in a number of neurological disorders, including migraine, epilepsy, and even some of the schizophrenia-like illnesses. Repeated ischaemic cell damage from vasospasm is also discussed as a possible factor initiating autoimmune disease and cancer. The similarities between viral transformation and neoplasia have led to the proposition that much cancer might be explained if as a species we have evolved by the gradual build-up of viruses.
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PMID:Stress and disease: the missing link. A vasospastic theory. III. Stress, vasospasm and general disease. 38 56

Mitogen-stimulated interleukin-2 (IL-2) production was measured in 122 patients who met Research Diagnostic Criteria for schizophrenia and 98 normal control subjects. The presence of autoantibodies against seven common antigens was also determined. There was no relationship between the presence of circulating autoantibodies and IL-2 production in control subjects. In patients, however, autoantibody-positive, acutely ill patients had significantly lower IL-2 production as compared with other patients and control subjects. Never-medicated patients showed the same trends for decreased IL-2 production in association with autoantibodies. These data suggest that decreased IL-2 production is associated with acute illness in schizophrenic patients who produce autoantibodies, a trait known to be associated with increased vulnerability to autoimmune disease.
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PMID:Altered interleukin-2 production in schizophrenia: association between clinical state and autoantibody production. 148 Jun 77

A number of assays were performed to assess immunologic function in 28 patients with clinically well-defined schizophrenia. Our data provide laboratory evidence that patients with schizophrenia have characteristics consistent with an autoimmune process, directed to components of the brain, which may participate in either the pathogenesis or etiology of schizophrenia. One-third of our patients had a clinically evident autoimmune syndrome unrelated to their psychiatric illness. Of the nine patients with an autoimmune disease, two had one autoantibody in their serum and five had more than one autoantibodies. Twelve of eighteen patients without clinical evidence of autoimmune disease had no detectable autoantibodies. Mitogenic responses to PHA and PWM were significantly reduced in the patient population when compared to controls. Fifty percent of the patients had an increased percentage (greater than 5%) of blood-borne HLA-DR (+) OKT4 (+) T-helper lymphocytes. Immune reactivity toward brain antigens was sought by measuring lymphocyte transformation to a saline extract of frontal lobe, and by immunoblotting of antigens extracted from frontal lobe, cingulate gyrus, interventricular septum, and hippocampus. Lymphocyte transformation did not reveal differences between patient and control groups. Normal sera were found to contain antibody to some of these brain antigens. However, patients with schizophrenia had antibody to antigens of the hippocampus, septal region and cingulate gyrus which were not encountered during analysis of normal sera.
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PMID:Clinical and laboratory evidence of autoimmunity in acute schizophrenia. 347 98

Schizophrenia shares several genetic features with diseases known to be autoimmune and could therefore be an autoimmune disease itself. Antipsychotic drugs, which are effective in treating the psychotic symptoms of schizophrenia, have one property in common--they block dopamine receptors in the central nervous system. This observation has led to the hypothesis that overactivity of dopaminergic pathways is the cause of the psychotic symptoms, but a seeming anomaly is that the turnover of dopamine is not increased in schizophrenia. Dopamine-receptor-stimulating autoantibodies are postulated to cause the dopaminergic hyperactivity, thereby accounting for the anomaly.
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PMID:Dopamine-receptor-stimulating autoantibodies: a possible cause of schizophrenia. 612 47

Autoimmunity has been shown to be the basis of an ever-increasing number of human diseases. Schizophrenia shares a number of genetic features with these autoimmune diseases and therefore could be an autoimmune disease itself. Several lines of evidence suggest that overactivity of dopaminergic pathways in some areas of the brain are involved in schizophrenia, but the apparent absence of an increase in dopamine turnover suggests that this hyperactivity could be mediated by a dopamine agonist rather than by dopamine itself. Schizophrenia is reviewed in the light of precedents from the field of autoimmune diseases in which autoantibodies have been shown to be able to interact with, and sometimes stimulate hormone receptors, thereby causing disease.
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PMID:Is schizophrenia an autoimmune disease? A review. 639 22

Heath and coworkers proposed that schizophrenia may be an autoimmune disorder in which antibodies are built up against specific substances in certain brain cells. Heath reports that schizophrenic patients exhibit abnormal brain waves in recordings from the caudate nucleus and septal area. These abnormal waves can also be recorded from similar sites in monkey brains after injections into the lateral ventricle cerebrospinal fluid of gamma-G-immunoglobulins (IgG) isolated from the blood of acutely ill schizophrenic patients. We prepared IgG fractions from control subjects and acutely ill schizophrenic patients and tested them in rhesus monkeys under double-blind conditions. Of 107 sera tested from 24 schizophrenic patients, 29 produced positive electroencephalographic recordings in the monkeys. From 30 control subjects we tested 80 samples and found 6 to be positive according to Heath's criteria. This amounts to more than 1 positive reaction for every 4 schizophrenic patients' fractions tested and approximately 1 positive in 13 from control subjects' serum fractions. The difference between control and patient groups is highly significant (p less than 0.001). Although our results confirm the experimental findings of the Heath group concerning abnormal EEG activity associated with an IgG fraction from schizophrenic patients, they differ from Heath's results for fractions from control persons. We found positive effects from a small number of control fractions whereas Heath claims never to have observed positive biological activity in control fractions. The autoimmune hypothesis has numerous drawbacks, the greatest of which is the inability to demonstrate the presence of circulating antibody in schizophrenic patients with the use of standard immunologic techniques.
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PMID:Immunologic studies in schizophrenic and control subjects. 718 73

Some patients with autoimmune disease have an elevation of the B lymphocyte population bearing the CD5 marker. In an attempt to replicate an earlier report of elevated CD5+ B cells in schizophrenic patients, lymphocytes were phenotyped in 116 patients with schizophrenia and 166 control subjects. The CD5+ B lymphocyte population was not elevated in medicated or never-medicated patients as compared with control subjects of similar age, race, gender, or social class. CD5+ B cells were also not elevated in patients who had circulating autoantibodies. The CD5+ B lymphocyte population was significantly elevated in African-American control subjects and patients in comparison with that in Caucasian control subjects and patients. Thus, although other immune alterations characterized a subset of patients with schizophrenia, an elevation of the CD5+ B lymphocyte population was not found in this study.
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PMID:CD5 positive B lymphocytes in schizophrenia: no alteration in numbers or percentage as compared with control subjects. 769 60

Autoimmune diseases aggregate in individuals and within pedigrees, and it has been postulated that autoimmune mechanisms may account for a proportion of schizophrenia. Structured questionnaires were used to interview the mothers of 121 DSM-III-R schizophrenic patients and the mothers of 116 controls in order to determine the prevalence of schizophrenia and of autoimmune diseases in their pedigrees. Patients with a schizophrenic first degree relative were significantly more likely to also have a parent or sibling with an autoimmune disease (60% vs. 20%, OR = 6.1, 95% CI = 2.3-6.5, p = 0.0003). A significant excess of insulin dependent diabetes mellitus (IDDM) was present in the parents and siblings of schizophrenic patients (OR = 9.65, 95% CI = 1.3-429.2, p = 0.009). These findings suggest that autoimmune mechanisms may play a role in the aetiology of schizophrenia, particularly familial schizophrenia. Associations have been established between autoimmune diseases and the HLA encoding genes of the major histocompatibility complex on chromosome six, and it may be that some of the genetic liability to schizophrenia involves these genes.
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PMID:Autoimmune diseases in the pedigrees of schizophrenic and control subjects. 882 52

Inbred MRL, NZB and BXSB strains of mice spontaneously develop a systemic, lupus-like autoimmune disease. The progress of autoimmunity is accompanied with a cascade of behavioral changes, most consistently observed in tasks reflective of emotional reactivity and the two-way avoidance learning task. Given the possibility that behavioral alterations may reflect a detrimental consequence of autoimmune-inflammatory processes and/or an adaptive response to chronic malaise, they are tentatively labeled as autoimmunity-associated behavioral syndrome (AABS). It is hypothesized that neuroactive immune factors (pro-inflammatory cytokines, brain-reactive antibodies) together with endocrine mediators (corticotropin-releasing factor, glucocorticoids) participate in the etiology of AABS. Since AABS develops natively, and has a considerable face and predictive validity, and since the principal pathway to autoimmunity is known, AABS may be a useful model for the study of CNS involvement in human autoimmune diseases and by extension, for testing autoimmune hypotheses of several mental disorders (major depression, schizophrenia, Alzheimer's disease, autism and AIDS-related dementia).
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PMID:Neurobehavioral alterations in autoimmune mice. 916 68

The strong negative correlation between schizophrenia and rheumatoid arthritis might provide clues as to the aetiology of these two diseases. An immunological explanation has been sought in the HLA sector of the major histocompatibility complex, which has been shown to have a role in the development of rheumatoid arthritis. The search for an association between schizophrenia and HLA haplotypes, however, has yielded only controversial results. Nevertheless, an autoimmune aetiology is still suspected. The recent demonstration of geographical co-occurrence of high rates of schizophrenia and flavivirus infection suggests, for the first time, that a natural resistance gene (NRG) might be involved in the aetiology of schizophrenia. Such a NRG is carried by the C3H/RV mouse, providing protection against lethal infection by flavivirus, but not by the histocompatible C3H/He mouse. Furthermore, the C3H/He mouse has proved to be a good model for the development of Lyme arthritis, resulting from infection by Borrelia burgdorferi. It is suggested that there is a possibility that the C3H/RV mouse, which is known to be resistant to both flavivirus and rickettsia, may also be resistant to borrelia, since the Ixodid tick vector of flavivirus is the vector for all three of these organisms. If so, then the C3H/RV mouse would resist infection by borrelia, and could not develop Lyme arthritis. It is hypothesised, therefore, that despite the histocompatibility of these two strains, while the C3H/He mouse is vulnerable to Lyme arthritis, the C3H/RV mouse may be resistant. As a consequence, NRGs may play a part in triggering autoimmune disease, with HLA antigens responsible for its further development. This would indicate that the negative association of schizophrenia and rheumatoid arthritis could result from resistance or vulnerability to certain infections.
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PMID:Schizophrenia, rheumatoid arthritis and natural resistance genes. 926 73


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