ReviewJournal of food and drug analysis2025
The rhythm of decline: Circadian disruption in neurodegeneration.
Review in Journal of food and drug analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
- Synchronizing immunity with time: unlocking the potential of chrono-immunotherapy in cancer.Frontiers in immunology · 2026Review
- Circadian Syndrome Mediates the Association Between Body Roundness Index and Incident Stroke Risk in Middle-Aged and Older Chinese Adults: A Nationwide Prospective Cohort Study.Behavioural neurology · 2026Article
- Current Strategies for Healthy Aging: The Interplay Between Nutrition, Metabolism, and Exercise.Cureus · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a multifactorial etiology involving genetic, environmental, and metabolic factors. Among these, circadian rhythm disruption has emerged as a crucial but under-explored contributor to disease progression. The circadian system, regulated by the suprachiasmatic nucleus (SCN), controls essential physiological functions such as the sleep-wake cycle, metabolism, and neuroendocrine signaling. Disruption of this system has been increasingly linked to key pathological features of AD, including amyloid-beta accumulation, tau hyperphosphorylation, and neuroinflammation. This review critically examines the mechanistic role of circadian misalignment in AD by analyzing studies on sleep disturbances, SCN degeneration, metabolic dysregulation, clock gene polymorphisms (BMAL1, CLOCK, PER, CRY), and gut-brain axis interactions. Evidence indicates that circadian abnormalities manifest as reduced melatonin secretion, impaired glymphatic clearance, and altered SCN signaling, all of which contribute to neuronal dysfunction and cognitive decline. Additionally, sleep deprivation has been shown to exacerbate amyloid-beta accumulation, while tau pathology can further disrupt circadian control, creating a vicious cycle. Dysregulated gut microbiota rhythms and associated metabolic changes further enhance neuroinflammatory responses, increasing AD risk. Diagnostic advances such as actigraphy, melatonin assays, and plasma biomarkers provide non-invasive methods for early detection of circadian misalignment. Therapeutic strategies targeting the circadian system-including light therapy, melatonin supplementation, and gene-based interventions-show promise in restoring circadian homeostasis and improving cognitive outcomes. Understanding and addressing circadian disruptions may offer novel and personalized approaches for delaying or mitigating Alzheimer's disease progression, highlighting the need for further research in this direction.
Indexed as
Identifiers
What OpenQuestion holds
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.