The influence of stress on neuroinflammation and alterations in brain structure and function in major depressive disorder

Yong Ku Kim, Eunsoo Won

    Research output: Contribution to journalReview articlepeer-review

    68 Citations (Scopus)

    Abstract

    Major depressive disorder (MDD) is a condition which has often been associated with chronic stress. The sympathetic nervous system is continuously activated without the normal counteraction of the parasympathetic nervous system under the influence of chronic stress. As a result, epinephrine and norepinephrine levels are increased, and acetylcholine levels are decreased, which in turn can increase the levels of pro-inflammatory cytokines. Peripheral inflammatory responses can access the brain, with neuroinflammation contributing to the increase in neurotoxic kynurenine pathway metabolites such as 3-hydroxykynurenine, 3-hydroxyanthranilic acid and quinolinic acid, and decrease in neuroprotective metabolites such as kynurenic acid. Pro-inflammatory cytokines can also exert direct neurotoxic effects on specific brain regions. Previous imaging studies have reported associations between pro-inflammatory states and alterations in brain regions involved in emotional regulation, including the hippocampus, amygdala and anterior cingulate cortex. Alterations in structure and function of such brain areas due to the neurotoxic effects of increased inflammation may be associated with the pathophysiology of depression. This review focuses the influence of stress on neuroinflammation which may cause alterations in brain structure and function in MDD.

    Original languageEnglish
    Pages (from-to)6-11
    Number of pages6
    JournalBehavioural Brain Research
    Volume329
    DOIs
    Publication statusPublished - 2017 Jun 30

    Keywords

    • Brain structure and function
    • Kynurenine pathway metabolites
    • Major depressive disorder
    • Neuroinflammation
    • Pro-inflammatory cytokines
    • Stress

    ASJC Scopus subject areas

    • Behavioral Neuroscience

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