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Aging is marked by cognitive decline, which in the case of Alzheimer’s disease is associated with tremendous global economic burden. Identifying modifiable risk factors for cognitive decline is therefore of paramount importance. In this chapter, we describe how aging compromises sleep quality and sleep architecture at a rate that parallels normal age-related cognitive decline. We argue that understanding the neurocognitive functions of sleep – frontal lobe restoration, memory consolidation, and metabolite clearance – and how such functions change in later life will be key to informing why some older individuals maintain healthy cognitive functioning and other older individuals do not. Critically, by investigating how sleep, cognition, and aging interact, researchers and clinicians can develop sleep-related treatments that target preventing, or at least ameliorating, pathologies such as Alzheimer’s disease.
This chapter focuses on primary sleep disorders in Parkinson's disease (PD) and multiple system atrophy (MSA) and insights provided by functional neuroimaging research. Specific disorders to be considered include excessive daytime sleepiness (EDS), sleep disordered breathing, restless legs syndrome/periodic limb movements in sleep (RLS/PLMS), and rapid eye movement (REM) sleep behavior disorder (RBD). The chapter reviews the relevant neurochemical pathways in PD and MSA, and discusses specific sleep disorders. It explains the neurotransmitter in more detail, as it relates to PD, MSA, and sleep circuits. The neurotransmitter dopamine may play a role in REM sleep control, but there is limited direct evidence for this. Dopamine may also play a role in regulation of the sleep/wake cycle with a wakefulness promoting effect that is similar to histamine and hypocretin. In the future, a greater focus should be placed on non-dopaminergic pathways to evaluate sleep disorders in PD and MSA.
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