Cognition-immune interactions between executive function and working memory, tumour necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNFR1 and sTNFR2) in bipolar disorder
Robson Zazula, Seetal Dodd, Olivia Dean, Michael Berk, Chiara C. Bortolasci, Waldiceu A. Verri, Heber Odebrecht Vargas, Sandra Odebrecht Vargas Nunes
Abstract
Objectives This study examined cognition-immune interactions, specifically executive function, working memory, peripheral levels of tumour necrosis factor-alpha (TNF-α), and soluble tumour necrosis factor receptors-1 and −2 (sTNFR1 and 2) levels in bipolar disorder (BD) patients in comparison with controls.Methods Thirty-one BD participants and twenty-seven controls participated in the study. The neurocognitive assessment was performed through three of CogState Research BatteryTM tasks for executive function and working memory. Plasma levels of TNF-α, sTNFR1, and sTNFR2 were measured after overnight fasting. Sociodemographic data and symptom severity of depression and mania were assessed.Results BD presented a significantly worse performance in the working memory task (p = .005) and higher levels of TNF-α (p = .043) in comparison to controls. A trend level of significance was found for sTNFR1 between groups (p = .082). Among BD participants, there were significant correlations between sTNFR2 and neurocognitive tasks (Groton Maze Learning Task: ρ = .54, p = .002; Set-Shifting Task: ρ = .37, p = .042; and the Two-Back Task: ρ = –.49, p = .005), and between sTNFR1 and mania, depression and anxiety symptoms (respectively ρ = .37, p = .038; ρ = –.38, p = .037; and ρ = .42, p = .002).Conclusion TNF-α and its receptors might be an important variable in cognitive impairment in BD. Future studies might focus on the development of anti-inflammatory therapeutic targets for cognitive dysfunction in BD.