Neuroimmune Mechanisms of Mood Disorder: A Translational Perspective

Po-See Chen, M.D, Ph.D.


Professor, Institute of Behavioural Medicine 
College of Medicine and Hospital 
National Cheng Kung University, Tainan, Taiwan



Psychosocial adverse conditions involving interpersonal processes are among the strongest proximal risk factors for mood disorders. A biologically plausible, multilevel theory that link experiences of social adverse condition with internal neuroimmune mechanisms that drive pathogenesis for mood disorders has been proposed. Central to this neuroimmune mechanism hypothesis is a novel axis of immune-to-brain bidirectional communication that influences mood and behavior. Under social adverse conditions, sympathetic nervous system can up-regulate myelopoiesis, monocyte trafficking and the expression of pro-inflammatory genes encoding a conserved transcriptional response to adversity (CTRA). The elevated pro-inflammatory cytokines caused by central microglia activation and recruitment of monocytes to the brain contributes to development of mood symptoms such as anhedonia, aggression, psychomotor retardation and social-behavioral withdrawal. Previous studies had suggested that the serum CRP levels are to be used as a biomarker for mood status and a predictor of treatment response in mood disorders. Clinical trials that used anti-inflammatory medications as adjunct pharmacotherapy in treating mood disorders. Besides, the neuroimmune mechanisms might link mood disorders with multiple system co-morbidities and sequential dementing change. Insights from this theory may thus shed light on understanding of immune-to-brain bidirectional communications, the role of psychosocial adverse conditions, the neuroimmune mechanisms of co-morbidities and late life consequence in mood disorders.