Role of sleep and neurochemical biomarkers in synaptic plasticity related to neurological and psychiatric disorders: A scoping review

Abstract

Sleep is vital for maintaining physical and mental well-being, impacting cognitive functions like memory and learning through neuroplasticity. Sleep disturbances prevalent in neurological and psychiatric disorders exacerbate cognitive decline, imposing societal burdens. Exploring the relationship between sleep and neuroplasticity elucidates the mechanisms influencing cognition, particularly amidst the prevalent sleep disturbances in these clinical populations. While existing reviews provide valuable insights, gaps remain in understanding the neurophysiological mechanisms underlying sleep and cognitive function. This scoping review aims to investigate the characteristic patterns of sleep parameters and neurochemical biomarkers in reflecting neuroplasticity changes related to neurological and psychiatric disorders and to explore how these markers interact and influence cognition at the molecular level. Studies involving adults and older adults were included, excluding animal models and the paediatric population. Selected studies explored the relationship between sleep parameter or neurochemical biomarker changes and cognitive impairment, reflecting underlying neuroplasticity changes. Peer-reviewed articles, clinical trials, theses, and dissertations in English were included while excluding secondary research and non-peer-reviewed sources. A three-step search strategy was executed following the updated Joanna Briggs Institute methodology for scoping reviews. Published studies were retrieved from nine databases, grey literature, expert recommendations, and hand-searching of the included studies' bibliography. A basic qualitative content synthesis of 34 studies was conducted per JBI's scoping review guidance. Slow-wave and Rapid-Eye Movement sleep, sleep spindles, sleep cycle disruption, K-Complex(KC) density, Hippocampal sEEG, BDNF, IL-6, iNOS mRNA expression, plasma serotonin, CSF Aβ-42, t-tau and p-tau proteins, and serum cortisol revealed associations with cognitive dysfunction. Examining the relationship between sleep parameters, neurochemical biomarkers, and cognitive function reveals neuronal mechanisms that guide potential therapeutic interventions and enhance quality patient care.