ArticleEvolution, medicine, and public health2017
Does selection for short sleep duration explain human vulnerability to Alzheimer's disease?
Article in Evolution, medicine, and public health, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 52 citations in OpenAlex.
- Systematic Review on the Association Between Sleep and the Risk of Alzheimer's Disease: An Evolutionary Perspective.Evolutionary applications · 2026Review
- Sleep deprivation: A risk factor for the pathogenesis and progression of Alzheimer's disease.Heliyon · 2024Review
- Pre-Diagnosis Sleep Status and Survival after a Diagnosis of Ovarian Cancer: A Prospective Cohort Study.Journal of clinical medicine · 2022Article
- Live fast, die young and sleep later: Life history strategy and human sleep behavior.Evolution, medicine, and public health · 2021Article
- 'Evolutionary medicine' perspectives on Alzheimer's Disease: Review and new directions.Ageing research reviews · 2018Review
- Circadian Rhythm and Alzheimer's Disease.Medical sciences (Basel, Switzerland) · 2018Review
- The Exceptional Vulnerability of Humans to Alzheimer's Disease.Trends in molecular medicine · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Compared with other primates, humans sleep less and have a much higher prevalence of Alzheimer 's disease (AD) pathology. This article reviews evidence relevant to the hypothesis that natural selection for shorter sleep time in humans has compromised the efficacy of physiological mechanisms that protect against AD during sleep. In particular, the glymphatic system drains interstitial fluid from the brain, removing extra-cellular amyloid beta (eAβ) twice as fast during sleep. In addition, melatonin - a peptide hormone that increases markedly during sleep - is an effective antioxidant that inhibits the polymerization of soluble eAβ into insoluble amyloid fibrils that are associated with AD. Sleep deprivation increases plaque formation and AD, which itself disrupts sleep, potentially creating a positive feedback cycle. These and other physiological benefits of sleep may be compromised by short sleep durations. Our hypothesis highlights possible long-term side effects of medications that reduce sleep, and may lead to potential new strategies for preventing and treating AD.
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.