Trouble Waking Up May Signal Slower Thinking in Older Adults, Study Finds

That groggy, disoriented feeling in the minutes and hours after waking—known to sleep scientists as sleep inertia—has long been treated as a minor nuisance, a brief fog that lifts with the first cup of coffee. A new study suggests it may deserve far more clinical attention, especially in later life. Researchers analyzing data from the long-running Wisconsin Sleep Cohort found that older adults who reported more severe sleep inertia performed measurably worse on standardized tests of cognitive function, even when those tests were administered many hours after they got out of bed. The findings, published in the Journal of Clinical Sleep Medicine, position sleep inertia as a potentially distinctive marker of brain health in aging, one that ordinary measures of daytime sleepiness failed to capture.

The study drew on 461 participants from the Wisconsin Sleep Cohort, a community-based longitudinal project that has tracked sleep health in Wisconsin adults since the late 1980s. For this analysis, the researchers used data collected between 2019 and 2023, when participants first completed the Sleep Inertia Questionnaire, a validated 23-item instrument that probes the cognitive, behavioral, emotional, and physiological dimensions of the sleep-to-wake transition. Participants averaged 73.8 years of age, were slightly more likely to be male, and were predominantly non-Hispanic white with at least some college education. Crucially, the cohort’s decades of infrastructure meant the researchers could adjust their statistical models for an unusually rich set of confounders, including body mass index, depression scores, alcohol and caffeine use, smoking history, chronotype, habitual sleep duration, and objectively measured sleep apnea severity from overnight polysomnography.

Cognitive performance was assessed with a standardized battery of six widely used neuropsychological tests, yielding seven outcome measures. The battery included the Rey Auditory Verbal Learning Test for memory, the Grooved Pegboard for fine motor speed and dexterity, Trail Making Test Part B for executive function and cognitive flexibility, the Symbol Digit Modalities Test for processing speed, the Controlled Oral Word Association Test for verbal fluency, and the Digit Cancellation Test for attention. Testing sessions lasted roughly 35 minutes and were deliberately scheduled during typical waking hours—usually late morning, mid-afternoon, or evening—rather than immediately upon awakening, with testing beginning an average of nearly 11 hours after participants reported waking on the day of assessment.

The results were striking in their selectivity. Higher scores on the Sleep Inertia Questionnaire were significantly associated with slower completion times on the Grooved Pegboard and Trail Making Test Part B, and with fewer correct responses on the Symbol Digit Modalities Test in unadjusted analyses. After the researchers statistically controlled for the full panel of demographic, psychosocial, and sleep-related covariates, the associations with the Grooved Pegboard and Trail Making Test Part B remained robust. These two tasks share a common thread: both depend heavily on psychomotor speed and executive functioning, suggesting that sleep inertia may be most closely tied to the brain’s capacity for rapid, coordinated, goal-directed processing rather than to memory or language abilities.

Perhaps the most intriguing finding was what did not predict cognition. The Epworth Sleepiness Scale, the gold-standard self-report measure of daytime sleepiness, showed no significant associations with any cognitive outcome. The Hypersomnia Severity Index, a broader measure of hypersomnia symptoms and impairment, produced only a single weak association—and it ran in a seemingly paradoxical direction, with greater hypersomnia severity linked to slightly better immediate verbal recall. The contrast implies that sleep inertia is not simply another face of general sleepiness. Instead, it appears to be a specific symptom with its own relationship to brain function, one that broader somnolence questionnaires may dilute or miss entirely.

Secondary analyses of the questionnaire’s four subscales sharpened the picture. The physiological, cognitive, and emotional subscales all showed significant associations with cognitive performance, particularly on the Grooved Pegboard and Trail Making Test Part B, with the physiological and cognitive subscales also linked to slower performance on the Digit Cancellation Test and reduced output on the Symbol Digit Modalities Test. The responses subscale, which captures behaviors such as waking to an alarm, showed no significant relationships—a pattern the authors attribute in part to the fact that most participants were retired and less likely to encounter the situations those items describe. Sensitivity analyses confirmed that the findings held when accounting for APOE4 carrier status, a major genetic risk factor for Alzheimer’s disease, and when excluding the small number of night-shift workers in the sample.

Why would the severity of morning grogginess relate to cognitive performance hours later? The biology of sleep inertia remains incompletely understood, but leading hypotheses center on the neural machinery of the sleep-to-wake transition itself. Awakening is not a single switch but a staggered cascade: brainstem arousal systems activate rapidly, while cortical regions—especially prefrontal areas supporting executive function—come online more slowly, and the functional segregation between task-positive and task-negative brain networks is temporarily lost. Proposed contributors include the slow clearance of sleep-promoting substances such as adenosine after waking, disrupted cortical arousal, circadian misalignment, and awakening from slow-wave sleep or during the biological night, all of which can intensify inertia. Pathologically severe sleep inertia, as seen in idiopathic hypersomnia, may reflect dysregulation of these transition mechanisms.

The connection to neurodegeneration is speculative but biologically plausible, and it is where the study becomes genuinely provocative. The locus coeruleus, the brain’s primary noradrenergic nucleus, is a key regulator of transitions between sleep and wakefulness and between REM and non-REM sleep—and it is among the earliest sites of pathological tau accumulation in Alzheimer’s disease, becoming hypoactive during preclinical stages. Impaired monoaminergic neurotransmission upon awakening could, in theory, mediate prolonged episodes of sleep inertia. Adding an intriguing circumstantial link, caffeine—an adenosine receptor antagonist—reduces sleep inertia in sleep-deprivation paradigms, increases locus coeruleus activity, and has been associated in epidemiological studies with diminished Alzheimer’s risk and better cognitive function. None of this establishes causation, but it sketches a coherent framework in which chronic, severe sleep inertia could serve as an early behavioral fingerprint of arousal-circuit vulnerability.

The authors are careful to frame the work as exploratory and preliminary. The cross-sectional design cannot determine whether sleep inertia contributes to cognitive decline, shares an underlying cause with it, or both. The sample, while large and well characterized, was predominantly white and non-Hispanic, limiting generalizability, and most cognitive testing occurred in the evening hours—though the models adjusted for hours since awakening, which the researchers argue makes it unlikely that the measured performance simply reflected acute grogginess during testing. The Sleep Inertia Questionnaire also relies on retrospective self-report, and because the analyses were exploratory, no correction for multiple comparisons was applied, leaving open the possibility that some associations reflect chance. Objective, ambulatory measures of sleep inertia and longitudinal designs in more diverse populations are the clear next steps.

Even with those caveats, the implications are tangible. Sleep inertia is a near-universal experience that typically dissipates within 30 minutes of waking, but its duration and intensity vary dramatically between individuals, and prolonged, debilitating inertia is a hallmark of idiopathic hypersomnia and a frequent complaint in obstructive sleep apnea, insufficient sleep syndrome, circadian rhythm disorders, and mood disorders. If replicated, the current findings suggest that a simple question about morning grogginess—how long it lasts, how severe it feels, how often it occurs—could be folded into clinical assessments of older adults as an inexpensive, readily obtainable signal of cognitive risk. They also raise the possibility that interventions designed to reduce sleep inertia, from optimized wake timing to pharmacological countermeasures, might one day help modify cognitive trajectories in aging. For now, the message is that the fog of waking up may be more than a nuisance: it could be a window into how the aging brain transitions between states of consciousness, and how well it will continue to perform.

Subject of Research: The association between sleep inertia severity and cognitive performance in older adults

Article Title: Association between sleep inertia and cognitive performance among older adults in the Wisconsin Sleep Cohort study

Article References: Love, J. J., Cook, J. D., Hagen, E. W., Rasmunon, A., Ravelo, L. A., Palta, M., Peppard, P. E., & Plante, D. T. (2026). Association between sleep inertia and cognitive performance among older adults in the Wisconsin Sleep Cohort study. Journal of Clinical Sleep Medicine, 22(1), Article 105. https://doi.org/10.1007/s44470-026-00133-4

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00133-4

Keywords: sleep inertia, cognitive performance, older adults, Wisconsin Sleep Cohort, hypersomnolence, executive function, psychomotor speed, neurocognitive testing, locus coeruleus, Alzheimer's disease, daytime sleepiness, sleep health