ArticleProceedings of the National Academy of Sciences of the United States of America2026
Cellular circadian period and its deviation associate with Alzheimer's pathology and brain aging in cognitively impaired older adults.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Timing the decline: Cellular circadian rhythms and Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
Corrections and comments
- Commented on by
Authors and funding
16 authors.
Funding
Abstract
Circadian rhythm disruption is recognized as a feature of aging and neurodegenerative disease, yet whether intrinsic cellular circadian properties relate to underlying processes in humans remains unknown. We measured intrinsic circadian period and its deviation from 24 h (Δ-period) using ex vivo bioluminescence in dermal fibroblasts from 135 older adults with cognitive complaints. Associations with plasma biomarkers (pTau-217, neurofilament light chain [NfL], and glial fibrillary acidic protein [GFAP]), amyloid positron emission tomography (PET), structural MRI, cognitive function, and clinical progression were examined within the amyloid-tau-neurodegeneration [ATN (IV)] framework, using multivariable models and Cox regression analyses. The median cellular circadian period was 24.2 h, while Δ-period increased with age. A longer intrinsic circadian period was selectively associated with higher pTau-217, NfL, and GFAP levels and medial temporal atrophy, consistent with Alzheimer's disease (AD)-related tau pathology, neurodegeneration, and glial activation. In contrast, greater Δ-period was associated with older age, poorer cognitive performance across multiple domains, and more widespread brain atrophy, consistent with broader aging-related neurodegenerative processes. Both longer period (HR = 4.41, 95% CI: 1.52 to 12.83) and greater Δ-period (HR = 2.65, 95% CI: 1.03 to 6.86) independently predicted faster clinical decline. Thus, cellular circadian period and Δ-period capture distinct biological processes-AD-related tau pathology vs. broader aging-related neurodegeneration-and together represent complementary cellular biomarkers with potential prognostic value in older adults with cognitive concerns.
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.