Published online by Cambridge University Press: 02 September 2021
Defining current psychopathology and optimum treatment selection in psychiatry relies solely on clinical symptom assessment but does not consider underlying biological correlates of psychiatric disorders. In particular, dysregulation of neurotransmitter metabolism and function (1,2), neuroendocrine pathways (3,4) and brain plasticity (5, 6) have been consistently reported across psychiatric disorders. Growing evidence points to a significant role of chronic low-grade inflammation in the pathophysiology of neuropsychiatric disorders such as major depressive disorder (MDD), schizophrenia (SCZ) and bipolar disorder (BD) (7–10). This features immune system dysfunctions including alterations in immune cell regulation (10), complement system (11–14), cytokine (15–18) and chemokine (7,8) pathways. As a result, current and conventional therapeutic strategies are not optimally positioned, with low remission and high relapse rates amongst individuals and treatment resistant numbers being high. Hence, the immune system is becoming a suitable target in personalizing treatment of psychiatric disorders. Unclear as yet is whether, unique immunological signatures exist for different psychiatric disorders including MDD, SCZ and BD and how these originate. Clearly a better characterization of the underlying biological aetiology will lead towards a more personalized and targeted approach.
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