Inflammation in Schizophrenia: Pathogenetic Aspects and Therapeutic Considerations

Norbert Müller


Schizophr Bull. 2018;44(5):973-982. 

In This Article


For a long time, little attention was paid to the potential involvement of an immunological process and consequent inflammation in the pathogenesis of schizophrenia. However, the evidence base for a range of relevant topics is growing, including the role of pro-inflammatory cytokines, the pronounced effects of pro- and anti-inflammatory cytokines on tryptophan/kynurenine metabolism; the effects of cytokines on glutamatergic neurotransmission; the results of imaging studies; the role of genetics; and the beneficial effects of anti-inflammatory drugs in schizophrenia. Despite this growing evidence, one must remember that immunological research is susceptible to interference from a range of factors, including medication, smoking, stress, and sleep. These factors cannot always be controlled, as can be seen from the example of stress: according to the vulnerability-stress-inflammation model, stress is not only a sine qua noncondition in schizophrenia but is also a confounding factor in studies of the immune response and inflammatory processes. The same applies to neuroimaging studies, ie, volume loss might be caused by pathological processes other than inflammatory ones.

Schizophrenia is hypothesized to be a syndrome with different underlying pathological processes. The same is true for inflammation, which has various stages and processes, ranging from acute to chronic and can also be an autoimmune process. Further research is needed to clarify the immune system's role in schizophrenia, in particular the relationship between inflammatory markers in the blood and CSF on the one hand and CNS volume loss on the other and also the relevance of different stages of inflammation for the disease. Nevertheless, recent findings, including the positive results of treatment studies, are encouraging and support continued research in this fascinating field.