Improved screening and treatments for sleep problems could help reduce the risk of Alzheimer’s disease (AD) in coming years when the number of cases of AD worldwide is expected to increase dramatically, wrote Erik S. Musiek, M.D., Ph.D., and Yo-El S. Ju, M.D., M.S.C.I., both of Washington University School of Medicine in a Viewpoint article in JAMA Neurology.
Accumulating data support a bidirectional association between AD pathology and sleep and circadian function. (The circadian rhythm, which is disrupted in sleep disorders, is the natural cycle of sleep and wakefulness.) “Despite the clear clinical need for therapeutic strategies to address sleep and circadian dysfunction, at the bedside we are stymied by lack of screening tools, prognostic markers, and most importantly, treatments to offer patients,” they wrote.
The authors noted that decreased sleep quality and fragmented circadian rhythms are associated with the development of AD as much as 15 years before symptoms begin to show. Moreover, large longitudinal studies show that obstructive sleep apnea and insufficient sleep increase risk of cognitive impairment.
The authors offered the following recommendations for advancing and translating sleep and circadian science into new strategies for AD prevention and treatment:
Basic Research
- Identify mechanisms linking sleep to the production and clearance in the brain of amyloid beta and tau, proteins that are associated with AD.
- Conduct studies to determine which aspects of sleep—sleep duration, specific sleep stages, or other variables—are most critical in AD pathogenesis.
- Examine the effects of different sleep- and circadian-promoting drugs or interventions on tau aggregation, inflammation, and other degenerative processes.
Clinical Research
- Conduct longitudinal studies beginning 20 years prior to the onset of cognitive symptoms that include sleep and circadian measures.
- Update existing longitudinal studies of aging and dementia to include the collection of sleep and circadian measures and enroll diverse cohorts to assess whether race and ethnicity may be associated with sleep and AD outcomes.
- Test the effect of existing treatments on cognitive outcomes, with specific attention to safety and tolerability.
- Identify and test new nonsedating therapies for sleep and circadian disruption in dementia patients.
“Greater implementation efforts are required to translate the emerging science on associations between sleep and circadian function and AD to benefit at the societal level,” Musiek and Ju wrote. For instance, evidence-based guidelines for sleep and circadian health behaviors, screening, treatment, and monitoring are needed and these guidelines need to be communicated to the public.
“A tsunami of AD looms in the coming 20 to 30 years, and sleep and circadian therapies that reduce AD risk would benefit societal health,” they continued. “To achieve such a goal, researchers in this area must intentionally adopt strategies to translate science efficiently and collaboratively into clinical trials and public implementation.”
For related information, see the Psychiatric News article “Sleep Loss Found to Exacerbate Spread of Toxic Protein Associated With Alzheimer’s Disease.”
(Image: iStock/Tero Vesalainen)
