Author(s): Morris JA
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Abstract The hypothesis proposed is that episodes of bacterial toxaemia occurring early in life cause subtle brain damage which predisposes to schizophrenia. The damage is most likely to occur in individuals who have one or more mutations in a large set of genes controlling aspects of the immune response to infection. These genes, numbering several hundreds or even thousands, control a vital but highly redundant system. Schizophrenia, by reducing fertility, causes selective pressure against the mutations which would otherwise accumulate in the genome and degrade our ability to fight infection. This hypothesis is consistent with the key features of the disease which include a strong genetic component, neuroanatomical abnormalities, a seasonal influence, lack of association with HLA subtypes and the observation that the frequency of schizophrenia is similar in widely different populations. If bacterial toxins also have a role in precipitating acute psychosis, then the age incidence of schizophrenia can be explained.
This article was published in Med Hypotheses
and referenced in Journal of Proteomics & Bioinformatics