Blood Proteins in Functional Psychoses

Fessel, W. J.

doi:10.1001/archpsyc.1962.01710200024004

Cited by 59 publications

(8 citation statements)

References 63 publications

(3 reference statements)

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“…The hypothesis that schizophrenia may be an immunological disease is longstanding. 3–5 Using the largest collection of genetic data currently available, we evaluated the immune hypothesis of schizophrenia empirically. We have shown that common variation at immune genes presents a very different genetic architecture in schizophrenia as compared to diseases of known immune origin.…”

Section: Discussionmentioning

confidence: 99%

“…Among many hypotheses of schizophrenia etiology, the longstanding immune theory posits that dysregulation of the immune system causes schizophrenia in at least a subset of patients. 3–6 It is known that immune components such as MHC class I, 7 TNF-α, 8 complement, 9 TGF-β, 10 and IL-6 11 regulate brain development and adult neural plasticity. Exposure to the wrong level of an immune factor at the wrong time may consequently disrupt brain development and adult neural functioning, as supported by in utero immune activation in rodents 12 and primates.…”

Section: Introductionmentioning

confidence: 99%

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Genome-Wide Association Studies Suggest Limited Immune Gene Enrichment in Schizophrenia Compared to 5 Autoimmune Diseases

Pouget¹,

Gonçalves

Spain

et al. 2016

SCHBUL

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There has been intense debate over the immunological basis of schizophrenia, and the potential utility of adjunct immunotherapies. The major histocompatibility complex is consistently the most powerful region of association in genome-wide association studies (GWASs) of schizophrenia and has been interpreted as strong genetic evidence supporting the immune hypothesis. However, global pathway analyses provide inconsistent evidence of immune involvement in schizophrenia, and it remains unclear whether genetic data support an immune etiology per se. Here we empirically test the hypothesis that variation in immune genes contributes to schizophrenia. We show that there is no enrichment of immune loci outside of the MHC region in the largest genetic study of schizophrenia conducted to date, in contrast to 5 diseases of known immune origin. Among 108 regions of the genome previously associated with schizophrenia, we identify 6 immune candidates (DPP4, HSPD1, EGR1, CLU, ESAM, NFATC3) encoding proteins with alternative, nonimmune roles in the brain. While our findings do not refute evidence that has accumulated in support of the immune hypothesis, they suggest that genetically mediated alterations in immune function may not play a major role in schizophrenia susceptibility. Instead, there may be a role for pleiotropic effects of a small number of immune genes that also regulate brain development and plasticity. Whether immune alterations drive schizophrenia progression is an important question to be addressed by future research, especially in light of the growing interest in applying immunotherapies in schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genome-Wide Association Studies Suggest Limited Immune Gene Enrichment in Schizophrenia Compared to 5 Autoimmune Diseases

Pouget¹,

Gonçalves

Spain

et al. 2016

SCHBUL

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“…Thus an increase in a 3 globulins by stress and STH may partly reflect an increase in plasma IgA. Fessel reviewed the studies on plasma protein changes in functional psychosis, and found that some of the changes reported in schizo phrenia are similar to plasma protein changes induced by stress (29).…”

Section: April 1974mentioning

confidence: 99%

Possible Interaction of Environmental and Biological Factors in the Etiology of Schizophrenia: Review and Integration

Strahilevitz¹

1974

Canadian Psychiatric Association Journal

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Possible interactions of genetic and environmental factors in the etiology of schizophrenia are discussed. Studies on the significance of genetic-constitutional and environmental factors in determining specificity of behavioural and biochemical responses to stressors in humans and experimental animals are reviewed. Studies of stress in schizophrenia are also revieweed and their possible relationships discussed. Hypotheses related to the interaction of environmental factors and genetic constitutional factors in the production of acute schizophrenic psychosis in genetically predisposed people are presented. Research studies supporting such hypotheses are reviewed and discussed. It is proposed that environmental pressures, by inducing a physiological state of stress or other biochemical physiological alterations, may be etiologically related to the development of acute schizophrenic psychosis by: • Producing chemical substances that act as inducers of enzymes, in particular transmefhylating enzymes and those involved in the production of proteins, which may be related to the etiology of schizophrenia; • Activating autoimmune processes which may be related to the etiology of schizophrenia; • Changing levels of brain amines; •Altering the permeability of the blood-brain barrier.

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“…He observed that immunoglobulin/protein in sera and cerebrospinal fluid from psychiatric patients may react with neuronal antigens (Lehmann-Facius, 1939). The above notion did not attract significant attention until the 60’s, when Fessel and Solomon published a series of reports on “macroglobulins” or “anti-brain factors” in psychotic patients (Fessel, 1962a, 1962b, 1962c; Fessel and Hirata-Hibi, 1963; Solomon, Moos, Fessel, and Morgan, 1966; Solomon, Allansmith, McCellan, and Amkraut, 1969). Although recent work supports the hypothesis that brain-reactive autoantibodies (BRAA) play a role in the pathogenesis of some forms of mental illness, further evidence is required to establish the cause-effect relationship (Ganguli et al, 1993; Tanaka et al, 2003; Schott, Schaefer et al, 2003; Margutti et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Circulating brain-reactive autoantibodies and behavioral deficits in the MRL model of CNS lupus

Williams

Šakić

Hoffman

2010

Journal of Neuroimmunology

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Brain reactive autoantibodies (BRAA) are hypothesized to play a role in the neuropsychiatric manifestations that accompany systemic lupus erythematosus (SLE). The present study tests the proposed relation between circulating BRAA and behavioral deficits in lupus-prone MRL/lpr mice. Two age-matched cohorts born at different times were used to test the relationship in the context of altered disease severity. Significant correlations between autoimmunity and behavior were detected in both cohorts. These results are the first to report correlations between behavior and autoantibodies to integral membrane proteins of brain, supporting the hypothesis that BRAA contribute to the behavioral dysfunction seen in lupus.

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Blood Proteins in Functional Psychoses

Cited by 59 publications

References 63 publications

Genome-Wide Association Studies Suggest Limited Immune Gene Enrichment in Schizophrenia Compared to 5 Autoimmune Diseases

Genome-Wide Association Studies Suggest Limited Immune Gene Enrichment in Schizophrenia Compared to 5 Autoimmune Diseases

Possible Interaction of Environmental and Biological Factors in the Etiology of Schizophrenia: Review and Integration

Circulating brain-reactive autoantibodies and behavioral deficits in the MRL model of CNS lupus

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