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.

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 Battery 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 ( = .005) and higher levels of TNF-α ( = .043) in comparison to controls. A trend level of significance was found for sTNFR1 between groups ( = .082). Among BD participants, there were significant correlations between sTNFR2 and neurocognitive tasks (Groton Maze Learning Task: ρ = .54,  = .002; Set-Shifting Task: ρ = .37,  = .042; and the Two-Back Task: ρ = -.49,  = .005), and between sTNFR1 and mania, depression and anxiety symptoms (respectively ρ = .37,  = .038; ρ = -.38,  = .037; and ρ = .42,  = .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.