Sleep Apnea’s Surprising Link to Alzheimer’s Disease

Poor Sleep and Brain Health

New research highlights the connection between sleep disturbances and neurodegenerative diseases like Alzheimer’s. Poor sleep can speed up the accumulation of harmful proteins in the brain. Sleep issues are emerging as early indicators of Alzheimer’s and Parkinson’s, making sleep a potential target for both diagnosis and treatment.

At the SLEEP Annual Meeting in Seattle, Ominigho Michael Bubu, MD, PhD, presented his research. He discussed how obstructive sleep apnea (OSA) impacts neurodegeneration and Alzheimer’s disease (AD).

Dr. Bubu examined the physiological, racial, and sex-based connections between OSA and AD in an interview. He explored how OSA mechanisms, such as reduced oxygen and fragmented sleep, might accelerate AD risk and progression. Marked differences were noted across racial and gender lines. Dr. Bubu also explored how OSA may contribute to amyloid and tau accumulation in the brain.

“Obstructive sleep apnea (OSA) is associated with increased Alzheimer Disease (AD) risk, with studies showing altered levels of both established and novel biofluid AD biomarkers in cross-sectional and longitudinal analyses.”

—Ominigho Michael Bubu, MD, PhD

OSA’s Varying Impact

Black/African American and Hispanic individuals face twice the sleep deprivation risk, with the highest rates of symptomatic OSA, especially excessive daytime sleepiness, compared to non-Hispanic white individuals. Men experience OSA more frequently than women. Studies indicate women, regardless of age or weight, have less severe OSA, shorter events, and more respiratory effort-related arousal (RERA) events compared to men.

Findings suggest older Black/African American and Hispanic adults had a higher risk for AD related to hypoxia and sleep duration. Women showed a greater AD risk linked to sleep fragmentation, while men faced an increased risk from hypoxia. The effects of sleep fragmentation and duration on AD risk were similar across races and sexes.

Dr. Bubu‘s research suggests that OSA, particularly through mechanisms related to hypoxia, sleep fragmentation, and sleep duration, might explain AD-related disparities.

OSA’s Role in Brain Changes

OSA may play a role in AD. It can contribute to neuronal injury through intermittent hypoxemia. It can accelerate Aβ and tau accumulation, increasing AD progression risk. OSA may also work synergistically with Aβ, increasing MCI/AD progression risk and impacting biomarker changes. Sleep fragmentation can affect time spent in Slow Wave Sleep (SWS), potentially impairing glymphatic clearance of amyloid and tau.

The public should be aware of the link between sleep problems and cognitive decline, including Alzheimer’s disease. Roughly 15% of Alzheimer’s cases could be linked to sleep issues. Addressing sleep problems could significantly reduce Alzheimer’s risk, particularly among Black and Hispanic patients. Providers should prioritize patient education on sleep and treatments.

OSA severity correlates with amyloid burden increases in cognitively normal older adults. Patients with OSA, both cognitively normal and with MCI, have an increased rate of worsening brain amyloid burden. Those with OSA show greater amyloid burden and altered brain volume. This may signify inflammation initially, with neurodegeneration occurring as the disease progresses.

Screening for OSA may benefit Alzheimer’s trials. OSA acts as an AD risk modifier, potentially accelerating AD biomarker changes. Combining OSA treatments with AD-specific therapies could optimize treatment outcomes. According to the CDC, approximately 30% of U.S. adults experience symptoms of insomnia. (CDC)