英文摘要 |
Since the 1980s, the “immune hypothesis of schizophrenia” has been suggested to associate immune dysfunction and neuroinflammation with schizophrenia, and a remarkable number of studies have shown the rôle of “immune dysregulation in schizophrenia”. The “mild encephalitis hypothesis of schizophrenia” proposed by the German researchers Bechter and Müller is one of the most promising new research concepts, suggesting that subgroups of patients with schizophrenia have a mild, but chronic, form of encephalitis with markedly different etiologies ranging from viral infections to autoimmune dysfunction. Modern psychoneuroimmunology has tried to associate infectiontriggered autoimmune dysfunction with risk factors for developing schizophrenia. Autoimmune psychosis is referred to the condition that a patient has atypical schizophrenia-like symptoms after autoimmune encephalitis, suggesting that the infection triggers autoimmune dysfunction. Such inflammation-triggered autoantibodies or dysregulation of T- and B-cell autoantibodies against a number of receptors, ion channels, and associated proteins causes the patients to present themselves with neurologic and psychotic symptoms. Till the year 2016, 16 kinds of neuronal cell surface antibodies have been introduced to cause autoimmune encephalitis. |