Sleep Apnea May Increase Alzheimer’s Risk in Older Adults, Study Finds
Summary: New longitudinal research reports a link between obstructive sleep apnea (OSA) severity and increasing amyloid beta accumulation in the brains of cognitively normal older adults.
Source: ATS
Obstructive sleep apnea (OSA) may raise the risk of developing Alzheimer’s disease (AD) in older adults, according to a new study published in the American Journal of Respiratory and Critical Care Medicine by the American Thoracic Society.
In the study entitled “Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly: A Longitudinal Study,” researchers tracked biomarkers associated with Alzheimer’s pathology—specifically amyloid beta (AB) peptides—and found that AB-related markers increased over time in older adults with OSA in proportion to the measured severity of their sleep-disordered breathing. In short, participants who experienced more apneas per hour showed greater accumulation of brain amyloid across the study period.
The authors note that Alzheimer’s disease is a progressive neurodegenerative disorder affecting millions of older adults, while OSA is highly prevalent among the elderly, with estimates ranging from about 30 to 80 percent depending on diagnostic criteria. Because OSA and AD share many risk factors and often coexist, establishing a direct association between OSA severity and amyloid accumulation has been challenging. This study aimed to examine that relationship longitudinally in a carefully screened cohort of cognitively normal older individuals.
The research included 208 participants aged 55 to 90 who demonstrated normal cognitive performance on standardized evaluations. The sample excluded individuals referred from sleep clinics, those already using CPAP therapy, people with depression, and those with medical conditions that could affect brain function. To measure Alzheimer’s biomarkers, investigators collected cerebrospinal fluid (CSF) by lumbar puncture to quantify soluble AB levels and, for a subset of participants, used positron emission tomography (amyloid PET) to directly visualize and quantify amyloid deposits in the brain.
Results showed that over half of the participants had OSA: 36.5 percent with mild OSA and 16.8 percent with moderate to severe OSA. A follow-up subgroup of 104 participants was reassessed after two years. In that longitudinal sample, greater OSA severity correlated with a decline in CSF AB42 levels over time—a pattern consistent with increased amyloid deposition in brain tissue. This pattern was corroborated in the subset who underwent amyloid PET imaging, which revealed increasing amyloid burden in those with OSA.
Interestingly, despite clear biomarker changes, the study did not find that OSA severity predicted measurable cognitive decline in this cohort over the study interval. Study coauthor Andrew Varga, MD, PhD, suggested this points to biomarker changes occurring during preclinical stages of Alzheimer’s disease—before cognitive symptoms emerge. The investigators caution that the absence of detectable cognitive decline may relate to the study’s relatively short duration, the participants’ high educational levels, and the limitations of standard cognitive tests to detect subtle or sleep-dependent changes.
The research team highlights the clinical implications of their findings. Given the high prevalence of undiagnosed OSA among older adults and the observed link between OSA and early amyloid accumulation, effective treatment of sleep apnea—such as CPAP therapy, oral appliances, positional therapy, and other interventions—could potentially delay or reduce the risk of later cognitive impairment and dementia for some individuals. The authors emphasize the importance of improved screening for OSA in older populations who are often asymptomatic, noting that early detection and treatment might carry significant benefits for brain health.
Limitations of the study include its observational design, which does not prove causation, the relatively short follow-up period for capturing cognitive decline, and a participant pool that may not represent the general population in terms of education and other demographic factors. The investigators call for longer and larger trials to determine whether treating OSA can slow amyloid accumulation or delay onset of cognitive symptoms.
Funding: Supported by the National Institutes of Health, the Foundation for Research in Sleep Disorders, the American Sleep Medicine Foundation, and the Friedman Brain Institute.
Source: Dacia Morris – ATS
Publisher: Organized by NeuroscienceNews.com
Image Source: Image credit: ATS.
Original Research: Full research PDF for “Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly: A Longitudinal Study” is available online from the publishing journal.
ATS. “Sleep Apnea May Increase Alzheimer’s Risk.” NeuroscienceNews. NeuroscienceNews, 10 November 2017.
Summary: This longitudinal study links obstructive sleep apnea severity to increases in amyloid beta biomarkers and PET-detected amyloid burden in cognitively normal older adults, suggesting that screening and treatment of OSA in the elderly may hold promise as part of strategies to preserve brain health and reduce dementia risk.