Evidence map›Paper›PMID 28217760›Full record

ArticleNeurobiology of sleep and circadian rhythms2017

Sleep in Alzheimer's Disease - Beyond Amyloid.

Jerrah Holth, Tirth Patel, David M Holtzman

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of sleep and circadian rhythms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.

  1. Pooled it
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  5. Observational
  6. Hypothalamic MCH neurons links tau pathology to sleep disruption.bioRxiv : the preprint server for biology · 2026
    Article
  7. Article
  8. Longitudinal association between sleep and Alzheimer's pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jerrah HolthDepartment of Neurology, Hope Center for Neurological Disorders, and the Knight Alzheimer's Disease Research Center, Washington University, 660 S. Euclid Ave, Box 8111, St. Louis, MO 63108.
Tirth PatelDepartment of Neurology, Hope Center for Neurological Disorders, and the Knight Alzheimer's Disease Research Center, Washington University, 660 S. Euclid Ave, Box 8111, St. Louis, MO 63108.
David M HoltzmanDepartment of Neurology, Hope Center for Neurological Disorders, and the Knight Alzheimer's Disease Research Center, Washington University, 660 S. Euclid Ave, Box 8111, St. Louis, MO 63108.
Hope Center for Neurological Disorders · US

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI RICHARD Justin PERRIN · 1985 to 2026
$69.5M
Viral Vectors CoreP01NS074969 · NINDS · WASHINGTON UNIVERSITY · PI SNIDER, BARBARA JOY · 2012 to 2021
$13.0M
The Relationship Between Tau Pathology and Sleep in TauopathiesF32NS089381 · NINDS · WASHINGTON UNIVERSITY · PI HOLTH, JERRAH KATHLEEN · 2014 to 2016
$164k
NIA NIH HHS P01 AG003991NINDS NIH HHS F32 NS089381NINDS NIH HHS P01 NS074969
6 · The paper itself

Abstract

Sleep disorders are prevalent in Alzheimer's disease (AD) and a major cause of institutionalization. Like AD pathology, sleep abnormalities can appear years before cognitive decline and may be predictive of dementia. A bidirectional relationship between sleep and amyloid β (Aβ) has been well established with disturbed sleep and increased wakefulness leading to increased Aβ production and decreased Aβ clearance; whereas Aβ deposition is associated with increased wakefulness and sleep disturbances. Aβ fluctuates with the sleep wake cycle and is higher during wakefulness and lower during sleep. This fluctuation is lost with Aβ deposition, likely due to its sequestration into amyloid plaques. As such, Aβ is believed to play a significant role in the development of sleep disturbances in the preclinical and clinical phase of AD. In addition to Aβ, the influence of tau AD pathology is likely important to the sleep disturbances observed in AD. Abnormal tau is the earliest observable AD-like pathology in the brain with abnormal tau phosphorylation in many sleep regulating regions such as the locus coeruleus, dorsal raphe, tuberomammillary nucleus, parabrachial nucleus, and basal forebrain prior to the appearance of amyloid or cortical tau pathology. Furthermore, human tau mouse models exhibit AD-like sleep disturbances and sleep changes are very common in other tauopathies including frontotemporal dementia and progressive supranuclear palsy. Together these observations suggest that tau pathology can induce sleep disturbances and may play a large role in the sleep disruption seen in AD. To elucidate the relationship between sleep and AD it will be necessary to not only understand the role of amyloid but also tau and how these two pathologies, together with comorbid pathology such as alpha-synuclein, interact and affect sleep regulation in the brain.

Indexed as

alpha-synucleinAlzheimer’s Diseasesleep, amyloidtau

Identifiers

PMID28217760
PMCPMC5312809
OpenAlexW2514003618

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.