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.
Keyphrases
- bipolar disorder
- genome wide
- immune response
- ankylosing spondylitis
- rheumatoid arthritis
- genome wide identification
- bioinformatics analysis
- multiple sclerosis
- systemic lupus erythematosus
- genome wide analysis
- disease activity
- drug induced
- gene expression
- clinical trial
- dna methylation
- toll like receptor
- spinal cord
- study protocol
- transcription factor
- white matter
- resting state
- functional connectivity
- microbial community
- cerebral ischemia
- systemic sclerosis
- open label
- intensive care unit
- interstitial lung disease
- high throughput sequencing