Summary: A new UC San Diego study finds that self-reported sleep complaints are an important risk factor for Alzheimer’s disease among older women who have a higher genetic predisposition. Drawing on data from the Women Inflammation Tau Study, researchers report that poor subjective sleep quality is linked to faster accumulation of tau protein in the brain and to declines in visual memory — but these associations were observed only in women with elevated genetic Alzheimer’s risk.
Because women represent nearly two-thirds of Alzheimer’s cases and often report poorer sleep than men, monitoring and addressing sleep quality in older women may offer a low-cost, non-invasive opportunity for earlier clinical intervention.
Key Findings
- Genetic dependence: The connection between poor sleep, memory decline, and tau accumulation appeared only in women with higher genetic risk for Alzheimer’s. Women with lower genetic risk showed no similar link.
- Specific cognitive impact: Poor sleep correlated with worse visual memory performance; verbal memory did not show the same association.
- Bidirectional relationship: Results support a feedback loop where disrupted sleep may accelerate tau buildup, and tau-related brain changes can further degrade sleep quality.
- Modifiable target: Because sleep quality can be improved through clinical and behavioral interventions, sleep represents a promising, actionable target for prevention strategies in at-risk older women.
Source: UCSD
Sleep complaints may be a meaningful Alzheimer’s disease risk factor in older women with higher genetic susceptibility, according to researchers at the University of California San Diego.
The study analyzed 69 women aged 65 and older who were enrolled in the Women Inflammation Tau Study, a longitudinal project focused on aging and Alzheimer’s disease risk. Participants completed validated sleep questionnaires, underwent standardized memory testing, and received PET brain scans that measured tau protein deposition, an Alzheimer’s hallmark.
Findings show that among women with higher genetic risk for Alzheimer’s, poorer self-reported sleep quality was associated with reduced visual memory performance and greater tau accumulation in brain regions affected early in the disease. By contrast, women with lower genetic risk did not demonstrate these relationships. The sleep-related effects were specific to visual memory and did not extend to verbal memory in this cohort.
The authors emphasize that these results support accumulating evidence for a bidirectional interaction between sleep disturbances and Alzheimer’s pathology. Prior research suggests deep sleep contributes to clearing metabolic byproducts, and chronic sleep disruption may therefore permit faster tau buildup. As tau accumulates and damages brain regions involved in sleep regulation, sleep quality may worsen further, creating a reinforcing cycle.
Given that older women report poorer subjective sleep more frequently than men and make up a majority of Alzheimer’s patients, the researchers argue that sleep complaints could serve as a useful clinical signal. Self-reported sleep measures are inexpensive and simple to administer, making them practical for identifying individuals who might benefit from closer monitoring or early interventions.
The research team suggests that improving sleep—through behavioral therapies, medical treatment of sleep disorders, or other evidence-based approaches—could become a targeted prevention strategy for Alzheimer’s, particularly for women with elevated genetic risk. The study highlights the potential importance of taking sleep-related complaints seriously in older women as part of broader brain health assessments.
Key Questions Answered
A: The study indicates that genetic risk moderates the impact of sleep complaints. Poor sleep alone did not uniformly produce Alzheimer’s-related changes; it appeared to act as an accelerating factor for pathology specifically in women who already carry higher genetic vulnerability.
A: Tau is a protein that can form abnormal tangles inside neurons in Alzheimer’s disease, disrupting neural circuits. Research points to a bidirectional mechanism: restorative deep sleep helps clear metabolic waste from the brain, so disrupted sleep may allow tau to accumulate more rapidly; conversely, tau-related damage to sleep-regulating regions can further degrade sleep quality.
A: Women bear a disproportionate share of Alzheimer’s diagnoses and frequently report poorer sleep than men. Because sleep is a potentially modifiable risk factor, studying older women offers a strategic opportunity to identify early intervention points for a population at higher overall risk.
Editorial Notes
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full by staff.
- Additional context was added by editorial staff.
About this Alzheimer’s and sleep research news
Author: Lizelda Lopez
Source: UCSD
Contact: Lizelda Lopez – UCSD
Image credit: 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. Banksl. Journal of Prevention of Alzheimer’s Disease. DOI: 10.1016/j.tjpad.2026.100581
Abstract
Background
Evidence increasingly points to a two-way relationship between sleep disturbances and Alzheimer’s disease (AD). Poor sleep may be an under-recognized risk factor for older women, who are disproportionately affected by AD and report worse subjective sleep than men. Higher genetic AD risk—measured here by a polygenic hazard score (PHS) that includes APOE ε4 status—might amplify the impact of disrupted sleep on AD-related measures, particularly in older women.
Objective
This study evaluated whether genetic AD risk moderates the relationship between subjective sleep complaints and both memory performance and tau burden in a sample 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), the Rey Auditory Verbal Learning Test, and the Brief Visuospatial Memory Test–Revised. They underwent [18]F-MK6240 PET scans to quantify tau burden across composite Braak-stage regions. Genetic risk groups were defined by the PHS stratified at the 75th percentile. Interactions between PSQI global scores and PHS group were tested for associations with memory composites (N = 69) and tau burden (N = 63).
Results
Significant interactions between PSQI score and PHS group were observed for visual memory and tau accumulation in Braak regions III/IV. Among women with higher genetic risk, poorer subjective sleep correlated with worse visual memory and increased limbic tau deposition. No significant associations were found for verbal memory or for tau in Braak regions I/II or V/VI.
Conclusion
Older women who report sleep problems and carry higher genetic risk for Alzheimer’s may face greater vulnerability to visual memory deficits and tau accumulation in regions affected early in AD. These results suggest that sleep complaints could serve as an actionable risk indicator, and that improving sleep may be a viable prevention strategy for at-risk older women.