Abstract
Mild encephalitis (ME) hypothesis suggested a usually smouldering in any case low level inflammatory process in the CNS resulting in a variety of psychopathological symptoms: indeed increased proinflammatory markers like cytokines have been described in blood and CSF in patients suffering from affective or schizophrenic disorders. Animal models showed that a hit in early life to the immune system might trigger a life-long increased immune reactivity respectively vulnerability. Many epidemiological and clinical studies show the role of various infectious agents as risk factors for schizophrenia with overlap to other psychoses. The first large scale epidemiological study in psychiatry from Denmark clearly demonstrates in severe infections and autoimmune disorders during lifetime as risk factors. Genetic studies detected several risk genes in a region related to immune functions. The vulnerability–stress model matches with ME hypothesis as stress may increase proinflammatory cytokines and even contribute to lasting proinflammatory state. The immune system itself is considered an important further piece in the puzzle like in autoimmune disorders in general which are always linked to three factors: genes, environment, immune system. Alterations of dopaminergic, serotonergic, noradrenergic and glutamatergic neurotransmission have been shown with low level neuroinflammation and may directly be involved in symptom generation. Volume loss, altered brain structure and microglial activation have been demonstrated in both types of psychoses in neuroimaging studies which matches with the assumption of a low level neuroinflammatory process. Further support comes from the therapeutic benefit of anti-inflammatory medications in specific studies and only recently recognized anti-inflammatory and immunomodulatory intrinsic effects of anti-depressants and neuroleptics.
Published Version
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