Citation

Stoddard-Bennett T, Lee JH. J. Suicidol. (Taipei) 2023; 18(3): 613-623.

Copyright

(Copyright © 2023, Taiwanese Society of Suicidology, Publisher Airiti)

DOI

10.30126/JoS.202309_18(3).0003

PMID

unavailable

Abstract

Bipolar disorder (BD) is a severe psychiatric condition characterized by mood lability, which poses the highest risk of suicide of any psychiatric illness. BD patients exhibit chronic neuroinflammation, especially during mood episodes, affecting cytokine levels in both the central nervous system and peripheral circulation. Genetic and environmental factors can trigger or exacerbate neuroinflammation, with disrupted sleep patterns and stressful life events being significant environmental triggers. This, in turn, leads to glial activation, mitochondrial disruption, and oxidative stress. Dysfunctional kynurenine and oxidative stress pathways have been implicated in the inflammatory process in BD, leading to synaptic deficits and neuronal loss associated with mood regulation and impulsivity. Evidence suggests that lithium confers neuroprotective effects and reduces suicide rates in BD. Other potential anti-inflammatory modulators such as ketamine have also shown efficacy in reducing suicidal ideation or managing BD symptoms. While treatments and lifestyle interventions targeting neuroinflammation may show promise in the future, further research is needed to understand the complex interplay between inflammation, mood, and suicidal behavior in BD. Efforts to identify personalized treatments considering individual neuroinflammatory profiles are crucial in improving outcomes for BD patients, particularly those at high risk for suicidal behavior. Overall, this narrative review highlights emerging evidence of neuroinflammation as one of the key pathophysiologies in BD and discusses new treatments targeting neuroinflammation to reduce the severity of mood symptoms and suicide rates in this vulnerable population.

Language: en