Evidence map›Paper›PMID 28145081›Full record

ArticleCNS neuroscience & therapeutics2017

Chronic Sleep Restriction Induces Cognitive Deficits and Cortical Beta-Amyloid Deposition in Mice via BACE1-Antisense Activation.

Hong-Yi Zhao, Hui-Juan Wu, Jia-Lin He, Jian-Hua Zhuang, Zhen-Yu Liu, Liu-Qing Huang, Zhong-Xin Zhao

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. β-Amyloid accumulation in the human brain after one night of sleep deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2018
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  15. The Reciprocal Interaction Between Sleep and Alzheimer's Disease.Advances in experimental medicine and biology · 2021
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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

7 authors at 1 institution in 1 country.

Hong-Yi ZhaoDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Hui-Juan WuDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Jia-Lin HeAcademy of Clinical Medicine, Second Military Medical University, Shanghai, China.
Jian-Hua ZhuangDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zhen-Yu LiuDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Liu-Qing HuangDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zhong-Xin ZhaoDepartment of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo clarify the correlation between chronic sleep restriction (CSR) and sporadic Alzheimer disease (AD), we determined in wild-type mice the impact of CSR, on cognitive performance, beta-amyloid (Aβ) peptides, and its feed-forward regulators regarding AD pathogenesis.

methodsSixteen nine-month-old C57BL/6 male mice were equally divided into the CSR and control groups. CSR was achieved by application of a slowly rotating drum for 2 months. The Morris water maze test was used to assess cognitive impairment. The concentrations of Aβ peptides, amyloid precursor protein (APP) and β-secretase 1 (BACE1), and the mRNA levels of BACE1 and BACE1-antisense (BACE1-AS) were measured.

resultsFollowing CSR, impairments of spatial learning and memory consolidation were observed in the mice, accompanied by Aβ plaque deposition and an increased Aβ concentration in the prefrontal and temporal lobe cortex. CSR also upregulated the β-secretase-induced cleavage of APP by increasing the protein and mRNA levels of BACE1, particularly the BACE1-AS.

conclusionsThis study shows that a CSR accelerates AD pathogenesis in wild-type mice. An upregulation of the BACE1 pathway appears to participate in both cortical Aβ plaque deposition and memory impairment caused by CSR. BACE1-AS is likely activated to initiate a cascade of events that lead to AD pathogenesis. Our study provides, therefore, a molecular mechanism that links CSR to sporadic AD.

Indexed as

Amyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesCerebral CortexCognition DisordersDisease Models, AnimalDNA, AntisenseEnzyme-Linked Immunosorbent AssayMaleMiceMice, Inbred C57BLReaction TimeRNA, MessengerSleep DeprivationAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseDNA, AntisenseRNA, MessengerBACE1BACE1-antisenseBeta-amyloidChronic sleep restrictionSporadic Alzheimer disease

Identifiers

PMID28145081
PMCPMC6492718
OpenAlexW2584909754

What OpenQuestion holds

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Registered trials

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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.