Sleep Improvement: A Preventative Therapy to Reduce the Risk for Cognitive Decline

Louise N Pivac

As the societal and economic impact of cognitive impairment increases with the ageing population, finding preventative measures to lower the risk of cognitive decline and pathological brain ageing is crucial. While suboptimal sleep is commonly reported by older adults, it is also a well-established comorbidity of Alzheimer's disease (AD), the most prevalent form of dementia. However, evidence suggests that sleep changes might occur before measurable cognitive impairment. Evidence suggests a bidirectional relationship whereby suboptimal not only results from but also contributes to AD related neuropathological change, subsequently increasing risk of cognitive decline and dementia. In addition to further investigating the bidirectional relationship, this thesis includes a world first investigation of sleep improvement as a preventative intervention. Firstly, a critical literature review was undertaken including an investigation of interventions available for sleep improvement and associations with cognition or neurobiological outcomes. Three longitudinal studies were conducted to further elucidate the relationship between self-reported sleep, cognitive performance and brain health. Self-reported sleep duration <6 hours and sleep efficiency <65%, were associated with accelerated attention and processing speed decline (Study 1). These aspects of self-reported sleep were also associated with faster accumulation of brain beta-amyloid (A), representing a potential underlying mechanism through which suboptimal sleep may influence cognition (Study 2). Important differences were observed in these relationships (Study 1 and Study 2) based on Apolipoprotein E ε4 allele carriage. Study 3 revealed that suboptimal sleep contributes to early reactive astrogliosis and a previously unseen decline in plasma glial fibrillary acidic protein (GFAP) during the preclinical period. Specifically, high self-reported risk of obstructive sleep apnoea and high baseline brain A burden were independently associated with higher plasma GFAP at baseline and predicted a negative plasma GFAP trajectory over time. Finally, our intervention study (Study 4) revealed world first preliminary evidence that improving suboptimal sleep is associated with preserved cognitive function, especially for individuals with a high brain A burden. Specifically, a greater improvement in self-reported sleep duration or sleep efficiency in individuals with high brain A at baseline, was associated with improved executive function performance at 18-month follow-up. Ultimately, findings from this thesis provide substantial new evidence for suboptimal sleep as a risk factor for cognitive decline and pathological brain ageing. Moreover, it offers evidence that improving suboptimal sleep could have immediate clinical benefits. Sleep improvement represents a non-invasive, cost-effective standard treatment that could aid a large segment of the population at risk of cognitive decline due to suboptimal sleep.

Sleep Improvement: A Preventative Therapy to Reduce the Risk for Cognitive Decline

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