Summary: After a single night without sleep, levels of the tau protein in blood rose by about 17% in healthy young men.
Sleep loss linked to short-term rise in blood tau — a biomarker associated with Alzheimer’s disease
Source: Uppsala University
A preliminary crossover study from researchers at Uppsala University reports that one night of total sleep deprivation produced a measurable increase in blood levels of total tau (t-tau) in healthy young men compared with a full night of sleep. The study, published in the journal Neurology, suggests that even brief sleep loss alters circulating biomarkers tied to brain health, highlighting a potential pathway by which disrupted sleep could affect long-term dementia risk.
Tau is a neuronal protein that, when it aggregates into tangles, is a hallmark of Alzheimer’s disease pathology. Tangles of tau can begin accumulating in the brain many years before clinical symptoms of Alzheimer’s appear. Previous research has shown that sleep disruption in older adults can raise tau levels in cerebrospinal fluid, and traumatic brain injury can elevate tau in blood. This new study extends those observations to younger, healthy adults under controlled laboratory conditions.
“Many people experience occasional sleep deprivation from jet lag, shift work, or late-night demands,” said study author Jonathan Cedernaes, MD, PhD, of Uppsala University. “Our exploratory findings indicate that missing a single night of sleep leads to a modest but detectable increase in tau in the blood of otherwise healthy young men. If such disturbances occur repeatedly over years, they might contribute to negative effects on brain health.”
The trial enrolled 15 healthy men with an average age of 22 who typically reported seven to nine hours of good-quality sleep nightly. Each participant completed two study conditions in randomized order while staying in a sleep clinic under standardized meals and sedentary activity: one condition involved two consecutive nights of normal sleep, and the other involved a normal first night followed by a full night of sleep deprivation. Blood samples were drawn in the evening before and in the morning after each condition. During the night of sleep deprivation, lights were kept on and participants remained awake, engaging in quiet activities such as movies, games, and conversation.
The investigators observed an average 17% increase in plasma total tau from evening to morning after the night of sleep loss, compared with only about a 2% change following normal sleep. The study also measured four other blood biomarkers related to neurodegeneration and glial response — amyloid-beta 40 (Aβ40), amyloid-beta 42 (Aβ42), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) — but found no significant differences between the sleep and sleep-deprived conditions for those markers.
Interpreting higher blood tau after sleep loss remains complex. “An increase in circulating tau could indicate enhanced neuronal release during wakefulness, or it might reflect increased clearance of tau from the brain into the blood,” Cedernaes explained. The present data do not resolve whether the rise in blood tau is harmful, compensatory, or transient. Additional studies are required to determine how long these blood changes persist, whether repeated sleep disruption produces cumulative effects, and whether blood tau dynamics link sleep disturbances to greater dementia risk over time.
The authors emphasize several limitations. The sample size was small and limited to young, healthy men, so findings may not generalize to women, older adults, or clinical populations. The study design cannot fully separate sleep loss effects from circadian influences, nor can it establish long-term consequences. Larger, more diverse cohorts and longer follow-up are needed to clarify mechanisms, the role of genetic and lifestyle factors, and potential implications for occupations that involve chronic sleep disruption such as shift work.
Source:
Uppsala University
Media Contacts:
Jonathan Cedernaes – Uppsala University
Image Source:
The image is in the public domain.
Original Research (closed access):
“Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men.” Christian Benedict, Kaj Blennow, Henrik Zetterberg, Jonathan Cedernaes. Neurology. DOI: 10.1212/WNL.0000000000008866.
Study abstract (summary)
Objective:
To determine whether a single night of sleep loss alters daily patterns of plasma biomarkers associated with Alzheimer’s disease and central nervous system health.
Methods:
In a randomized, two-condition crossover protocol, 15 healthy young men completed standardized in-laboratory sessions comparing normal sleep to overnight sleep deprivation. Plasma assays measured total tau, Aβ40, Aβ42, NfL, and GFAP in fasting evening and morning samples using ultrasensitive assays.
Results:
Sleep loss increased the evening-to-morning ratio of total tau by about 17% compared with a 1.8% change after normal sleep (statistically significant). No significant sleep-related differences were observed for Aβ40, Aβ42, NfL, or GFAP. Across both conditions, Aβ42 and GFAP showed an overall evening-to-morning decrease.
Conclusions:
This exploratory study indicates that acute sleep deprivation raises blood t-tau in young men, supporting the idea that even short-term sleep loss can affect markers of brain health. Larger studies are needed to separate sleep and circadian effects, assess long-term consequences, and examine interactions with genetic and lifestyle risk factors.