Citation

Postolache TT, Manalai P, Brenner LA, Brundin L. Adv. Biol. Psychiatry (Basel) 2015; 30: 123-144.

Copyright

(Copyright © 2015, Karger)

DOI

10.1159/000434746

PMID

unavailable

Abstract

Clinical and epidemiological data accumulated over the past decade strongly suggest that inflammation, certain upstream triggers of the immune system and downstream molecular mediators of inflammation, may contribute to the pathophysiology of suicidal behavior. Upstream factors include autoimmune factors, infections, traumatic brain injury, and stress. Downstream factors potentially mediating the effects of inflammation include molecules of the kynurenine pathway, which are known to modulate neuroinflammation and glutamate neurotransmission. The following could contribute to an important rejuvenation of our suicide prevention arsenal: (1) targeting immune dysregulation in patients with a history of suicidal behavior; (2) preventive factors involving upstream activators such as chronic latent infections or allergens and, (3) interrupting downstream pathophysiological pathways of inflammation. Additionally, the focus on individual triggers and diatheses will increase the precision of our treatment interventions in suicide prevention. Finally, it might be possible to increase the accuracy of suicide risk estimation by adding analysis of inflammatory biomarkers to our clinical information and neuropsychological testing. Discovering novel agents that target inflammation may also rejuvenate our therapeutic interval in suicide prevention.

Language: en