Associations between wearable-device-measured daytime and nighttime light exposures and dementia risk: A prospective cohort study.

Overview

1. Institute of Neuropsychiatry, The Affiliated Brain Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China
2. Key Laboratory of Sleep and Biological Rhythms of Guangdong Province, Center for Sleep and Circadian Medicine, The Affiliated Brain Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China
3. Guangdong Engineering Technology Research Center for Translational Medicine of Mental Disorders, Guangzhou, Guangdong, China
4. School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China
5. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University of London, London, UK
6. Li Chiu Kong Family Sleep Assessment Unit, Department of Psychiatry, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China
7. Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China
8. Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, Jiangsu, China
9. Department of Big Data in Health Science, Zhejiang University School of Public Health and Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
10. Molecular Neuropharmacology, Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden
11. State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China

Abstract

Background: Identifying reliable predictors for dementia remains a critical unmet need. Light exposure plays a crucial role in regulating circadian rhythms, which influence cognitive function. However, the association between light exposure and dementia risk remains unclear.

Aims: This study examined the associations of daytime and nighttime light exposure with dementia risk.

Methods: A total of 87 577 dementia‐free participants (mean age: 62.36 years; 56.98% female) were included. Daytime and nighttime light exposures were measured using 7‐day free‐living wrist‐worn accelerometry. Incident dementia was identified from primary care, hospital inpatient admissions and death registry data. Cox proportional hazards models assessed associations, and mediation analyses evaluated circadian rest–activity rhythms (CRARs), brain structures and vitamin D as potential mediators.

Results: Over a median follow‐up of 8.1 years, 741 participants developed dementia. Daytime light exposure above 1000 lux was associated with reduced dementia risk (hazard ratio [HR] 0.84, 95% confidence interval [CI] 0.71–0.99, p = 0.039). Longer exposure to brighter light (e.g., ≥ 0.70 h at ≥ 5000 lux; HR 0.83, p = 0.036) was associated with a further reduction in risk. In exploratory analyses, CRARs and brain structures mediated up to 33% of the association. Protective associations were stronger in those with high levels of nighttime light exposure, an evening chronotype or apolipoprotein E (APOE) ε4 carrier status, with a risk reduction of up to 41%. Furthermore, < 0.70 h per day of bright daytime light (≥ 5000 lux) outperformed six established dementia predictors (e.g., obesity, alcohol consumption, traumatic brain injury and so on). Nighttime light showed no significant association with dementia risk.

Conclusions: High levels of daytime light exposure were significantly associated with lower dementia risk. Further research should explore its role in dementia screening and inform the development of light‐based interventions.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

• ams.ukbiobank.ac.uk/ams — at UK Biobank; found in “DATA AVAILABILITY STATEMENT”

Data availability statement

All data supporting the UKB study were obtained from the UK Biobank. The use of UK Biobank data has been approved by the UK Biobank Research Team (Application ID: 58082). Researchers who wish to access the data must follow the official procedure for data application from the UK Biobank (https://ams.ukbiobank.ac.uk/ams/).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 14 authors, 7 keywords, 70 references.

Cite

This paper

Zheng, N., Wang, W., Li, B., Mei, X., Liu, Y., Du, J., Chan, N. Y., Chan, J. W. Y., Xing, X., Tan, X., Benedict, C., Wing, Y. K., Zhang, J., & Feng, H. (2026). Associations between wearable-device-measured daytime and nighttime light exposures and dementia risk: A prospective cohort study. General psychiatry, 39(3), e70039. https://doi.org/10.1002/gps3.70039

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1038/s41538-026-00914-4

Green tea catechin EGCG attenuates hippocampal atrophy and cognitive impairment in obesity via autophagy signaling.

Journal: NPJ science of food

In common: ams.ukbiobank.ac.uk/ams, 1 reference

[2] doi:10.1016/j.isci.2026.115994

High intensity 40 Hz flicker improves amyloid pathology and cognition with autophagy in 3xTg mice.

Journal: iScience

In common: Alzheimer's / dementia, 3 references

[3] doi:10.1093/sleep/zsag041

Dim light at night impacts circadian rhythms and Alzheimer's disease-like neuroinflammation and neuropathology in humanized APP SAA knock-in mice.

Journal: Sleep

In common: Alzheimer's / dementia, 3 references

[4] doi:10.1007/s12031-026-02506-z

Striatal Dysregulation of Angpt2 and Circadian Gene Expression in a Rotenone Rat Model of Parkinson's Disease.

Journal: Journal of molecular neuroscience : MN

In common: 3 references

[5] doi:10.1186/s13024-026-00948-y

Dual orexin receptor antagonism with lemborexant enhances microglial clearance of β-amyloid in mice.

Journal: Molecular neurodegeneration

In common: Alzheimer's / dementia, 2 references

[6] doi:10.3390/jcm15176822

Predictors of Six-Month Functional Outcome After Chronic Subdural Hematoma Surgery: Logistic Regression Versus Machine Learning.

Journal: Journal of clinical medicine

In common: clinical / translational, 2 references

[7] doi:10.1093/cercor/bhag105 [code]

The tangential growth of the human visual cortex and maternal smoking during pregnancy.

Journal: Cerebral cortex (New York, N.Y. : 1991)

In common: 3 references

[8] doi:10.1186/s11556-026-00410-4

Not just how much, but how it's done: movement activity bout distributions and everyday cognition in older adults with elevated dementia risk.

Journal: European review of aging and physical activity : official journal of the European Group for Research into Elderly and Physical Activity

In common: Alzheimer's / dementia, 2 references

[9] doi:10.1038/s41467-026-71252-y

Genetic architecture of sleep in a genome wide association study of device measured sleep traits.

Journal: Nature communications

In common: 2 references

[10] doi:10.1186/s13073-026-01698-8 [code]

From aging to Alzheimer's disease: concordant brain DNA methylation changes in late life.

Journal: Genome medicine

In common: Alzheimer's / dementia, clinical / translational, 2 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.