ReviewFrontiers in neuroscience2025
Mechanism study of exercise intervention on circadian disruption in Alzheimer's disease.
Review in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research advances in physical activity and insomnia: a bibliometric and thematic evolution analysis.Frontiers in psychiatry · 2026Pooled it
- The Neuroprotective Role of Exercise in Alzheimer's Disease: An Integrative Review of Animal and Human Studies.Neurology international · 2026Review
- Exercise-induced modulation of astrocyte in Alzheimer's disease: mechanisms and therapeutic implications.Frontiers in physiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) induces profound circadian disruption-characterized by suprachiasmatic nucleus (SCN) degeneration, Aβ and tau pathology, and aberrant melatonin secretion which results in fragmented sleep-wake cycles and cognitive decline. Emerging evidence indicates that exercise significantly ameliorates these circadian rhythm and sleep-wake disturbances through multiple mechanisms. Specifically, exercise accelerates the removal of Aβ and tau by activating autophagy-lysosomal degradation and glymphatic clearance, thereby reducing the neuropathological burden. Furthermore, exercise also upregulates neuroprotective pathways and strengthens the amplitude and phase stability of core clock gene oscillations, which in turn restores robust melatonin rhythmicity and SCN function. Collectively, these effects break the vicious cycle between AD pathology and circadian disruption, stabilizing circadian homeostasis and improving cognitive function. These mechanistic insights highlight exercise as a robust non-pharmacological chronotherapeutic strategy for ameliorating circadian disruption in AD. These insights support the development of personalized, chronotype-tailored exercise interventions to resynchronize circadian rhythms and ultimately improve sleep quality and cognitive function in patients with AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.