Sleep quality mediates the relationship between systemic inflammation and neurocognitive performance

Rachel R Jin; Carman Nga-Man Cheung; Clive H Y Wong; Chelsea C W Lo; Crystal P I Lee; Hing Wai Tsang; Preeti Dinesh Virwani; Patrick Ip; Kui Kai Lau; Tatia M C Lee

doi:10.1016/j.bbih.2023.100634

Sleep quality mediates the relationship between systemic inflammation and neurocognitive performance

Brain Behav Immun Health. 2023 May 5:30:100634. doi: 10.1016/j.bbih.2023.100634. eCollection 2023 Jul.

Authors

Rachel R Jin^{1

2}, Carman Nga-Man Cheung³, Clive H Y Wong⁴, Chelsea C W Lo³, Crystal P I Lee³, Hing Wai Tsang⁵, Preeti Dinesh Virwani³, Patrick Ip⁵, Kui Kai Lau^{1

6}, Tatia M C Lee^{1

2}

Affiliations

¹ State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong, China.
² Laboratory of Neuropsychology and Human Neuroscience, The University of Hong Kong, Hong Kong, China.
³ Department of Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
⁴ Department of Psychology, The Education University of Hong Kong, Hong Kong, China.
⁵ Department of Paediatrics and Adolescent Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
⁶ Division of Neurology, Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.

Abstract

Background: Systemic inflammation is a significant mechanism underpinning adverse cognitive changes. Sleep quality is a crucial factor associated with systemic inflammation and neurocognitive health. Elevated levels of pro-inflammatory cytokines in the periphery help mark inflammation. With this background, we examined the relationship between systemic inflammation, subjective sleep quality, and neurocognitive performance in adults.

Method & results: In 252 healthy adults, we measured the systemic inflammation reflected by serum levels of IL-6, IL-12, IL-18, TNF-α and IFN-γ, subjective sleep quality reflected by the global scores of the Pittsburgh Sleep Quality Index, and their neurocognitive performance measured by the Hong Kong Montreal Cognitive Assessment. We observed that neurocognitive performance was negatively related to IL-18 (p = 0.046) and positively related to sleep quality (p = 0.006). We did not observe significant associations between other cytokines and neurocognitive performance. Furthermore, we found that sleep quality as a mediator explained the relationship between IL-18 and neurocognitive performance depending on the levels of IL-12 (index of moderated mediation: 95% CI = [0.0047, 0.0664]). Better subjective sleep quality buffered the negative effect of IL-18 on neurocognitive performance when IL-12 was low (bootstrapping 95% CI: [- 0.0824, - 0.0018]). On the contrary, poor subjective sleep quality mediated the association between higher IL-18 and poorer neurocognitive performance when IL-12 was elevated (bootstrapping 95% CI: [0.0004, 0.0608]).

Conclusion & implications: Our findings indicate that systemic inflammation was negatively associated with neurocognitive performance. Sleep quality regulated by IL-18/IL-12 axis activation could be a potential mechanism underpinning neurocognitive changes. Our results illustrate the intricate relationships between immune functioning, sleep quality and neurocognitive performance. These insights are essential to understand the potential mechanisms underpinning neurocognitive changes, paving the way for the development of preventive interventions for the risk of cognitive impairment.

Keywords: Cognitive impairment; Human cognition; Inflammation; Sleep quality.