Citation

Donegan JJ, Nemeroff CB. Adv. Exp. Med. Biol. 2023; 1411: 379-404.

Copyright

(Copyright © 2023, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/978-981-19-7376-5_17

PMID

36949319

Abstract

Suicide is a leading cause of death worldwide. Although the neurobiological dysfunction underlying suicidal behavior remains unclear, recent work suggests that the immune system may play a role in the pathophysiology of suicide. In this chapter, we discuss a nascent body of literature suggesting that peripheral and central nervous systems (CNS) inflammation are associated with suicidal behavior. Because early-life stress is a major risk factor for suicidal behavior and is also associated with immune dysregulation, we hypothesize that such immune dysregulation may be the mechanism by which childhood maltreatment leads to an increased risk of suicidal behavior and suicide. Targeting inflammatory processes may be a novel treatment strategy, especially in populations that have experienced childhood trauma and exhibit elevated inflammation. Future work should directly test the hypothesis that reducing inflammation would result in a reduction in suicidal behavior.

Language: en

Keywords

Humans; Risk Factors; Suicide; Suicidal Ideation; Inflammation; Microglia; *Suicide; Astrocyte; Early-life adversity; IL-1β; IL-6; Immune System; Kynurenine pathway; TNF-α