Inflammation and inflammatory processes within the body have been linked to the pathology of schizophrenia, particularly the activity of microglia cells, which are the primary immune cells of the central nervous system.[Howes & McCutcheon, 2017; Melborne et al., 2017]
In one study, the role of microglia in schizophrenia was interrogated using PET to image microglial activity in the brains of individuals identified as being at ‘ultra high risk’ of developing psychosis, as assessed on the Comprehensive Assessment of the At-Risk Mental States (CAARMS), as well as in patients with schizophrenia.[Bloomfield et al., 2016] The study found a correlation between microglial activity and being at ultra high risk of developing psychosis (Cohen’s d effect size of 1.2).[Bloomfield et al., 2016] This effect was specific to schizophrenia and was not seen in patients with depressive symptoms.[Bloomfield et al., 2016] Studies of this nature can struggle to separate the potential effect of antipsychotic treatment on the brain from the underlying pathology of schizophrenia, which is why it is powerful to include patients who have developed schizophrenia, as well as patients who are deemed to be at ultra high risk of developing psychosis, as determined on the CAARMS scale.[Bloomfield et al., 2016]
References:
Bloomfield PS, Selvaraj S, Veronese M, et al. Microglial activity in people at ultra high risk of psychosis and in schizophrenia: an [11C] PBR28 PET brain imaging study. Am J Psychiatry 2016; 173 (1): 44–52.
Howes O, McCutcheon R. Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization. Transl Psychiatry 2017; 7: e1024.
Melborne JK, Feiner B, Rosen C, Sharma RP. Targeting the immune system with pharmacotherapy in schizophrenia. Curr Treat Options Psychiatry 2017; 4 (2): 139–151.