Summary: A new study finds that self-reported sleep complaints are a significant risk factor for Alzheimer’s disease in older women who carry a higher genetic predisposition. Using data from the Women Inflammation Tau Study, researchers show that poorer sleep quality is linked to faster accumulation of tau protein and declines in visual memory — but these links appear only in women with elevated genetic risk.
Because women represent nearly two-thirds of Alzheimer’s cases and often report worse sleep than men, monitoring sleep quality could provide a low-cost, noninvasive way to identify at-risk individuals and guide early intervention strategies.
Key Facts
- Genetic dependency: The connection between poor sleep, visual memory decline, and tau aggregation was observed only in women with high genetic risk for Alzheimer’s; women with lower genetic risk did not show this pattern.
- Specific cognitive impact: Poor sleep was associated specifically with worse visual memory performance; verbal memory did not show the same association.
- Bidirectional feedback: Findings support a feedback loop in which disrupted sleep may accelerate tau deposition, and tau-related brain changes may in turn further disrupt sleep.
- Modifiable target: Sleep quality is potentially amenable to clinical and behavioral improvements, making it an important, modifiable target for prevention in vulnerable groups.
Source: UCSD
Sleep complaints may be an important Alzheimer’s disease risk factor in older women with greater genetic susceptibility, according to research from the University of California San Diego.
The study reports that older women with higher genetic risk who described poorer sleep also demonstrated greater memory difficulties and more Alzheimer’s-related brain changes, measured by tau protein deposition.
Researchers analyzed 69 women aged 65 and older enrolled in the Women Inflammation Tau Study, a longitudinal project examining aging and Alzheimer’s risk. Participants completed validated sleep questionnaires, underwent memory assessments, and received positron emission tomography (PET) scans that quantify tau, a protein that accumulates abnormally in Alzheimer’s disease.
Results indicated that poorer self-reported sleep correlated with worse visual memory and higher tau burden in brain regions affected early in Alzheimer’s disease — and these associations were present only in women with elevated genetic risk. Women with lower genetic risk did not display the same links between sleep complaints, cognitive performance, and tau accumulation. The observed effect was specific to visual memory and was not found for verbal memory tests.
The findings add to accumulating evidence that sleep disturbance and Alzheimer’s pathology are interconnected. Prior research supports a model in which deep sleep helps clear metabolic waste from the brain; when sleep is disrupted, tau and other abnormal proteins may accumulate more readily. As tau accumulates and damages brain regions that regulate sleep, sleep quality can worsen further, forming a harmful cycle.
Given the disproportionate impact of Alzheimer’s on women and their higher reported rates of poor sleep, the authors emphasize that sleep quality may be an accessible and clinically relevant risk marker. Self-reported sleep assessments are inexpensive and easy to administer, suggesting they could help identify older women who would benefit from closer monitoring or early intervention.
The researchers propose that sleep improvement — whether through behavioral therapy, sleep hygiene, or medical treatment of sleep disorders — could become a focus for Alzheimer’s prevention strategies, especially for women with higher genetic risk. Overall, the study supports taking sleep complaints seriously in older women as a potentially meaningful indicator of brain health.
Key Questions Answered:
A: The study suggests an interaction with genetic vulnerability. Poor sleep alone does not necessarily cause Alzheimer’s changes; instead, it may act as a catalyst that triggers pathology in women who already carry an elevated genetic risk for the disease.
A: Tau is a protein that can form abnormal tangles inside neurons in Alzheimer’s disease, disrupting neural circuits. Deep sleep appears to promote clearance of metabolic waste from the brain, so chronic sleep disruption may permit tau to accumulate more rapidly. As tau damages regions involved in sleep regulation, sleep disturbances can worsen, creating a feedback loop.
A: Women make up a large majority of Alzheimer’s cases and tend to report poorer sleep quality than men. Studying women allows researchers to focus on a population that is both highly affected by the disease and potentially responsive to sleep-based prevention strategies.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full.
- Additional context was provided by the editorial staff.
About this Alzheimer’s disease and sleep research news
Author: Lizelda Lopez
Source: UCSD
Contact: Lizelda Lopez – UCSD
Image: The image is credited to Neuroscience News
Original Research: Open access. “Sleep complaints and genetic risk of Alzheimer’s disease in older women: associations with memory and tau deposition” by Kitty K. Lui, Xin Wang, Melanie A. Dratva, Ella T. Lifset, Jordan Stiver, Nadine C. Heyworth, Qian Shen, Michael Thomas, Pamela N. DeYoung, Atul Malhotra, Erin E. Sundermann, and Sarah J. Banks. Journal of Prevention of Alzheimer’s Disease. DOI: 10.1016/j.tjpad.2026.100581
Abstract
Background
Growing evidence points to a bidirectional relationship between sleep disturbances and Alzheimer’s disease (AD). Poor sleep may be an underrecognized risk factor for older women, who are disproportionately affected by AD and often report poorer subjective sleep quality than men. Elevated genetic AD risk — assessed by a polygenic hazard score (PHS) that includes APOE ε4 carriership — may amplify the effects of disrupted sleep on AD-related outcomes in older women.
Objective
This study tested whether genetic AD risk modifies the relationship between subjective sleep complaints and both memory performance and tau burden in a cohort of older women.
Participants
Participants were women aged 65 and older enrolled in the Women Inflammation Tau Study.
Measurement
Participants completed the Pittsburgh Sleep Quality Index (PSQI) and underwent cognitive testing (Rey Auditory Verbal Learning Test and Brief Visuospatial Memory Test–Revised) as well as [18]F‑MK6240 PET scans to quantify regional tau. Tau burden was calculated across composite Braak stage regions. Genetic risk groups were defined by polygenic hazard score (PHS) stratified at the 75th percentile. Interactions between PSQI global score and PHS group were examined for memory composites (N = 69) and tau burden (N = 63).
Results
Interactions between PSQI global score and PHS group were observed for visual memory and tau in Braak regions III/IV. Among higher genetic risk women, poorer subjective sleep related to worse visual memory and greater limbic tau deposition. No significant associations were found for verbal memory or tau in Braak regions I/II or V/VI.
Conclusion
Older women with elevated genetic risk for Alzheimer’s disease who report sleep difficulties may be more likely to show visual memory deficits and increased tau in regions affected early in AD. These results suggest that self-reported sleep complaints could serve as an accessible risk marker and that improving sleep may offer a potential intervention target for reducing AD risk in this vulnerable population.