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Could interventions to ensure a good night’s sleep help prevent Alzheimer’s disease?

Sleep disturbance appears to be a risk factor for and an early manifestation of Alzheimer’s disease (AD), so interventions to ensure a good night’s sleep might help prevent AD development and progression. This was the main message for a plenary audience at AAIC19.

Disturbed sleep should be a therapeutic target

An overview of the evidence associating deteriorating sleep patterns with the development of AD was presented at the plenary address and suggests that disturbed sleep should be a therapeutic target. However, although healthy sleep appears to be an AD risk reduction opportunity, it is not included in current recommendations for reducing AD risk and progression.

 

EEG sleep disturbances are associated with aging and AD

Slow wave activity (SWA) and sleep spindles support cognitive processes

Electroencephalographic studies have shown that aging is associated with typical topographical loss of power in two sleep waveforms —SWA and sleep spindles.1 These waveforms occur during non-rapid eye movement (NREM) sleep and are known to support cognitive processes such as learning and memory.1

Furthermore, amyloid-β (Aβ) burden in the medial prefrontal cortex has been found to correlate significantly with the severity of impairment in NREM SWA generation.2 The investigators responsible for this finding propose that the link between Aβ pathology and impaired NREM SWA suggests that sleep disruption might be a mechanistic pathway through which Aβ pathology contributes to hippocampus-dependent cognitive decline in the elderly.2

 

Sleep disturbances are associated with an increased risk of AD

Insomnia is associated with AD

A metanalysis of 18 studies involving 246,786 individuals found that those who reported sleep disturbances had a higher risk of incident all-cause dementia, AD, and vascular dementia than individuals without sleep disturbances; and insomnia in particular was related to AD.3

A further metanalysis of 27 studies involving 69,216 individuals demonstrated that the risk for AD and cognitive impairment was 1.68 times higher for those with sleep problems, and that approximately 15% of AD in the population may be attributed to sleep problems.4

Sleep-disordered breathing is a common cause of sleep disturbance and is associated with widespread brain injury, including damage to brain regions mediating emotion, mood, memory and cognitive functioning.5 It has been shown to be associated with cognitive decline at an earlier age.6

Sleep-disordered breathing is associated with earlier cognitive decline

 

Interventions to improve sleep quality might prevent the onset and progression of AD

The audience was advised that intervention to address sleep disturbance represents an AD risk reduction opportunity. However, little is known about the effectiveness of intervention, the type of intervention, and at what point of the AD time course it should be implemented, though it was suggested that addressing sleep disturbance should be an early intervention.

Until research can provide the answers to these questions, it was suggested that sleep hygiene (good sleep habits) and identifying and treating illnesses that might be disturbing sleep (such as depression, restless legs and sleep apnea) are appropriate measures to implement at present. In addition, potential therapeutic measures include hypnotics and reduced exposure to strong anticholinergic medications that are associated with an increased risk for dementia.7

Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References
  1. Sprecher K, et al. PLOS ONE 2016;11:e0149770.
  2. Mander B, et al. Nat Neurosci 2015;18:1015–17.
  3. Shi L, et al. Sleep Med Rev 2016;40:4–16.
  4. Bubu O, et al. Sleep 2017;40:1–18.
  5. Harper R, et al. Respir Physiol Neurobiol 2013;188(3):383–91.
  6. Osario R, et al. Neurology 2015;84:1964–71.
  7. Coupland C, et al. JAMA Intern Med 2019; doi:10.1001/jamainternmed.2019.0677.
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