The Role of Inflammation in the Pathophysiology of Schizophrenia
In this occasional feature on Psych Congress Network, members of the Psych Congress Steering Committee answer questions asked by audience members at Psych Congress meetings.
QUESTION: Does inflammation play a role in the pathophysiology of schizophrenia, and if so, is there a benefit from anti-inflammatory treatment?
ANSWER: It is safe to assume that inflammation is not a singular, and most likely not even the main, pathophysiological process underpinning development of schizophrenia. Furthermore, presence of dysregulated inflammatory signaling may not be equally influential in all phases of the illness. Nevertheless, there is an accumulation of clinical and preclinical evidence pointing to a relevant role of inflammation in the etio-pathogenesis of schizophrenia.
A recent study utilizing a clustering procedure noted that 40% of individuals suffering from schizophrenia displayed higher levels of cytokine mRNA expression, compared to only 21% of healthy controls.1 Dysregulated peripheral inflammatory signaling may precipitate a change in astrocyte and microglia function in the brain. Increased astrocyte tryptophan-dioxygenase activity may produce elevated kynurenine activity, with subsequent compromised glutamate transmission via NMDA, and cholinergic signaling via nicotinic receptors (kynurenine is a functional antagonist at NMDA-Rs and a7nAch-Rs). These alterations may be in part responsible for negative and cognitive symptoms of schizophrenia. Moreover, inflammation-induced microglial release of quinolinic acid may be responsible for excitotoxicity and neural damage in schizophrenia.2
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