Interplay between pro-inflammatory cytokines, childhood trauma, and executive function in depressed adolescents. (July 2019)

• Record Type: Journal Article
• Authors: Peters, Amy T.; Ren, Xinguo; Bessette, Katie L.; Goldstein, Benjamin I.; West, Amy E.; Langenecker, Scott A.; Pandey, Ghanshyam N.
• Is Part Of: Journal of psychiatric research. Volume 114(2019)
• Page Start: 1
• Page End: 10
• Publication Date: 2019-07
• Subjects: Depression -- Adolescence -- Inflammation -- Executive function -- Trauma; Psychiatry -- Periodicals; Mental Disorders -- Periodicals; Maladies mentales -- Périodiques; Psychiatry; Electronic journals; Periodicals; 616.89005
• DOI: 10.1016/j.jpsychires.2019.03.030
• Languages: English
• ISSNs: 0022-3956

Abstract

Abstract: Background: Pro-inflammatory cytokines have been linked to depression, early childhood trauma, and impairment in executive function in adults. Whether these links are present during adolescence, a time when vulnerability to depression is heightened, a point more proximal to childhood trauma, and a critical period of brain development, is not well understood. Method: Serum levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor alpha (TNF-α) were measured in 70 adolescents aged 12–17, including 40 with a DSM-IV depressive disorder (DEP), a sub-set (n = 22) of whom reported a history of childhood trauma (DEP-T), and 30 healthy controls (HCs). Participants completed performance-based (Parametric Go/No-Go Task) and observer-rated (Behavior Rating Inventory of Executive Function) measures of executive function. Procedures were conducted at a subspecialty clinic (Dec 2015–June 2017). Results: IL-6 was elevated in DEP and DEP-T adolescents compared to controls ( p = .014) and TNF-α was elevated in DEP participants only ( p = .040) compared to controls, whereas no group differences were found in IL-1β ( p = .829). Additionally, DEP-T participants demonstrated relative deficits in performance-based ( p = .044) and observer-rated inhibitory control ( p = .049) compared to controls. Across the whole sample, TNF-α was associated with performance-based ( r = −0.25, p = .039) and observer-rated ( r = 0.32, p = .009) inhibitory control deficits. In subgroup analyses, TNF-α was associated with increased observer-rated inhibitory deficits in DEP, and at the trend level, with reduced inhibitory control performance in DEP-T. Conclusions: The current results suggest that inflammation may be a marker of disease processes in adolescent depression. Though longitudinal studies are needed, depressed adolescents with childhood trauma exposure appear to constitute a uniquely vulnerable group in terms of objective risk for executive dysfunction. Immune dysregulation may partly contribute to this risk.