Alzheimer’s disease: Is sleeping too long a tell-tale sign?

July 23, 2026 5 min read 2

The earlier dementia — of which Alzheimer’s disease is the most common — is detected, the better the prognosis for the person diagnosed.

Although there is no cure, early diagnosis of Alzheimer’s can help to delay the progression of the disease, allow the use of disease-modifying treatments, such as lecanemab and donanemab where appropriate, and give patients and carers time to arrange appropriate care.

Several studies have linked sleep changes to the development of Alzheimer’s disease, and now a study has suggested a possible physiological mechanism underlying the link.

The new study, published in Alzheimer’s and Dementia, the journal of the Alzheimer’s Association, found that people who slept for an average of more than 8.5 hours a night had higher levels of the blood biomarker p-tau181, suggesting that long sleep may be an early sign of neurodegenerative changes.

Steven Allder, MD, a consultant neurologist at Re:Cognition Health, who was not involved in the study, told Medical News Today:

“This study strengthens growing evidence that changes in sleep may be linked to the earliest biological processes involved in Alzheimer’s disease, rather than simply being a consequence of aging. […] What is particularly interesting here is the association between longer sleep and higher levels of plasma phosphorylated tau (p-tau181), a biomarker that reflects Alzheimer’s pathology.”

Researchers analysed data from 2,410 participants in the Framingham Heart Study (FHS), who had a mean age of 70, give or take 8.45 years, and 55.2% of whom were female.

All participants had self-reported sleep duration data and assay results for at least one of four blood-based biomarkers: p-tau181, total tau (t-tau), neurofilament light chain (NfL), or glial fibrillary acidic protein (GFAP).

To assess the sleep-biomarker relationship across the cognitive spectrum, they included individuals with mild cognitive impairment, dementia, and any history of stroke.

The participants reported typical sleep duration to technicians during clinic visits, where they also gave fasting blood samples for biomarker analysis.

Researchers took several factors that may affect sleep and biomarkers into account during analysis:

They then performed statistical and sensitivity analyses to determine any links between sleep duration and blood biomarkers.

Of the cohort, 576 (23.9%) reported short sleep (up to and including 6 hours a night), 1,475 (61.2%) average sleep (6-9 hours), and 359 (14.9%) long sleep (more than 9 hours).

Those reporting longer sleep were older, and were more likely to have depression, use antidepressants and have dementia than average sleepers.

All biomarkers tended to increase with longer sleep duration, but the increase was significant only for p-tau181.

P-tau181 had a J-shaped curve, with short sleepers having more than average sleepers. It then increased steadily with more than 8.5 hours sleep, and increased sharply for people reporting 10 or more hours of sleep.

“While the findings do not prove causation, they add to the evidence that alterations in sleep may be an early clinical sign of underlying neurodegeneration and reinforce the role of considering sleep as part of an overall assessment of brain health,” Allder commented.

The authors suggested that longer sleep duration could be a sign of disturbed sleep, and Allder agreed:

“Sleep duration alone tells us very little about sleep quality. Someone spending nine or ten hours in bed may actually experience fragmented or inefficient sleep, repeatedly waking throughout the night without necessarily being aware of it. We know that deep, restorative sleep plays an important role in clearing waste products, including amyloid proteins, from the brain via the glymphatic system. Fragmented sleep may impair restorative processes,” he told Medical News Today.

“However,” he added, “it is equally possible that early Alzheimer’s pathology itself disrupts the brain regions that regulate normal sleep, meaning disturbed sleep could be both a contributor to, and a consequence of, the disease.”

“A lot of people worry about whether their sleep habits are affecting their brain health,” corresponding author Vanessa M. Young, PhD, MS, a postdoctoral research fellow at the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio, said in a press release.

“Because this is a snapshot in time rather than a long-term study, we cannot say that long sleep causes Alzheimer’s, but the findings suggest it may be worth monitoring, and that more sleep is not always better for brain health,” Young noted.

The observational study allowed researchers to identify a link, but not prove any causation between long sleep and p-tau181.

It is equally possible that the sleep changes are a result of early neurodegeneration, rather than a cause of it, as Allder explained.

According to him: “Many dementia specialists believe this is one of the most likely explanations. Alzheimer’s disease begins silently in the brain 15 to 20 years before symptoms appear, and the earliest pathological changes may affect areas involved in regulating the sleep–wake cycle. As a result, people may gradually begin sleeping for longer before they notice any memory problems.”

“To determine whether long sleep is a cause or an early symptom, researchers need prospective studies that recruit cognitively healthy individuals, measure Alzheimer’s biomarkers at baseline and then follow changes in sleep over many years,” he added.

“Dementia is influenced by a complex relationship of genetics, vascular health, lifestyle and aging. Sleep is one piece of that puzzle, and maintaining good sleep hygiene, alongside routine physical activity, cardiovascular risk reduction and cognitive stimulation, remains one of the most sensible strategies for promoting long-term brain health.”

– Steven Allder, MD