Leveraging Sleep to Preserve Cognitive Health, With Bryce Mander, PhD

Sleep disturbances and dementia share a complex, bidirectional relationship that may offer clinicians an important opportunity to preserve cognitive health, according to Bryce Mander, PhD, who presented the session "Sleep Impairment as a Modifiable Driver of Dementia: Neural, Glymphatic, and Clinical Pathways" at SLEEP 2026 in Baltimore, Maryland.

In an interview during the meeting, Mander highlighted emerging evidence suggesting that sleep impairment is not merely a symptom of neurodegenerative disease but may actively contribute to the development and progression of cognitive decline through multiple biological pathways.

"The way the brain expresses sleep is critical for supporting cognitive functions," Mander explained. "Different sleep disturbances can disrupt or magnify Alzheimer's disease biomarkers, while those same biomarkers can further disrupt the restorative qualities of sleep."

This reciprocal relationship creates what Mander described as a “vicious cycle.” Sleep disturbances may accelerate the accumulation or effects of Alzheimer's disease-related biomarkers, while those biomarkers impair the brain's ability to generate restorative sleep patterns necessary for memory consolidation, neural recovery, and cognitive function. Over time, these interactions may influence an individual's cognitive trajectory and dementia risk.

Although substantial attention has focused on pharmacologic approaches to reducing dementia risk, Mander noted that sleep itself represents a promising and potentially modifiable target.

"There are a number of sleep medications on the market with different targets," he said. While research is still needed to determine whether specific therapies can meaningfully reduce dementia risk among individuals with sleep disturbances, Mander expressed optimism about the possibilities. "The science hasn't been done yet to really show that, but I think there's a lot of possibilities to think about that we can be excited about."

For primary care clinicians, Mander emphasized the importance of recognizing and treating sleep disorders that frequently go undiagnosed, particularly obstructive sleep apnea.

According to Mander, sleep apnea remains underrecognized in women, in part because traditional risk factors and clinical presentations often differ from those seen in men. As a result, standard assessments may underestimate disease burden.

Because many women express their sleep apnea more in REM sleep than in non-REM sleep, he says overall measures of sleep apnea severity may suggest a relatively mild condition despite substantial REM-related disease.

This distinction may have important implications for brain health. Mander noted that sleep apnea occurring during REM sleep appears to have meaningful cognitive consequences, particularly among individuals already at elevated risk for dementia. He expressed concern that women with REM-predominant sleep apnea may be overlooked and undertreated, potentially missing opportunities to improve long-term cognitive outcomes.

The message for clinicians, he said, is to maintain a high index of suspicion for sleep disorders even when traditional screening measures appear reassuring.

Ultimately, Mander hopes clinicians increasingly view sleep as a core component of dementia prevention strategies rather than a secondary consideration.

"Sleep is a modifiable behavioral lifestyle factor, and sleep disorders are readily treatable," he said. "The more that we can focus on promoting sleep as one of those core pillars of health, the more I think we can improve cognitive lifespan and brain health and reduce risk for dementia."

As research continues to clarify the neural, glymphatic, and clinical mechanisms linking sleep and neurodegeneration, the field is moving toward a future in which optimizing sleep may become a routine component of preserving cognitive health across the lifespan.

Editors’ note: Mander reports relevant disclosures with Eisai Co and AstronauTx.

References

1. Mander B. Sleep impairment as a modifiable driver of dementia: neural, glymphatic, and clinical pathways. Presented at: SLEEP 2026; June 2026.

2. Lucey BP, Bateman RJ. Amyloid-β diurnal pattern: possible role of sleep in Alzheimer's disease pathogenesis. Neurobiol Aging. 2014;35(suppl 2):S29-S34. doi:10.1016/j.neurobiolaging.2014.03.035