The Autoimmune Model of SchizophreniaReportar como inadecuado

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ISRN PsychiatryVolume 2012 2012, Article ID 758072, 8 pages

Research Article

Faculty of Medicine, University of Otago, Box 913, Dunedin 9050, New Zealand

Division of Commerce, University of Otago, Dunedin 9054, New Zealand

Kimg’s College London, University of London, London SE1 8UB, UK

Received 25 January 2012; Accepted 26 February 2012

Academic Editor: C. Bonetto

Copyright © 2012 D. D. Adams et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Schizophrenia is of mysterious causation. It is not infectious, not congenital, but shows familial aggregation, the Mendelian genetics indicating involvement of multiple codominant genes with incomplete penetrance. This is the pattern for autoimmune diseases, such as Graves’ disease of the thyroid, where forbidden clones of B lymphocytes develop, and cause thyrotoxicosis by secreting autoantibodies that react with the thyroid gland’s receptor for thyroid-stimulating hormone from the pituitary gland. In 1982, Knight postulated that autoantibodies affecting the function of neurons in the limbic region of the brain are a possible cause of schizophrenia. Today, this is even more probable, with genes predisposing to schizophrenia having being found to be immune response genes, one in the MHC and two for antibody light chain V genes. Immune response genes govern the immune repertoire, dictating the genetic risk of autoimmune diseases. The simplest test for an autoimmune basis of schizophrenia would be trial of immunosuppression with prednisone in acute cases. The urgent research need is to find the microbial trigger, as done by Ebringer for rheumatoid arthritis and for ankylosing spondylitis. This could lead to prophylaxis of schizophrenia by vaccination against the triggering microbe.

Autor: D. D. Adams, J. G. Knight, and A. Ebringer



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