Inflammation in suicidality: implications for novel treatment options.

Abstract

Suicide is an increasing health problem worldwide and the most severe complication of multiple psychiatric disorders. It is also prevalent in several somatic conditions. In recent years, significant advances have been made in understanding the neurobiology of suicidal behaviors. Several lines of evidence have emerged suggesting that inflammation may contribute to the pathophysiology of suicide. Basic and clinical data indicate that the effects of inflammation on mood and behavior are likely to be mediated by the kynurenine pathway metabolites and glutamatergic neurotransmission. At the same time, the triggers of inflammatory changes observed in suicidal patients are largely unknown but may include stress, infectious agents and autoimmune diseases. As available treatment options against suicidality are only moderately effective, targeting the inflammatory system may provide novel therapeutic opportunities. For this goal to be achieved, however, we need to gain better insight into the origin, mechanisms and outcomes of inflammation in suicidal behavior.