Evidence map›Paper›PMID 31244649›Full record

ReviewFrontiers in aging neuroscience2019

Sleep, Aging, and Cellular Health: Aged-Related Changes in Sleep and Protein Homeostasis Converge in Neurodegenerative Diseases.

Jennifer M Hafycz, Nirinjini N Naidoo

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Increased rates of brain protein synthesis during [N1,N2] sleep: L-[1-Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Sleep and Cellular Stress.Current opinion in physiology · 2020
    Article
  15. Sleep and ageing: from human studies to rodent models.Current opinion in physiology · 2020
    Article
  16. Article
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

2 authors at 2 institutions in 1 country.

Jennifer M HafyczCenter for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Pennsylvania, PA, United States.
Nirinjini N NaidooCenter for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Pennsylvania, PA, United States.
Circadian (United States) · USUniversity of Pennsylvania · US

Funding

Training in Sleep & Sleep DisordersT32HL007953 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI David Menassah Raizen, AMY M SAWYER · 2000 to 2026
$10.6M
Cellular and Molecular Basis of Sleep Loss Neural Injury in Alzheimer DiseaseR01AG064231 · NIA · UNIVERSITY OF PENNSYLVANIA · PI NAIDOO, NIRMALA NIRINJINI, VEASEY, SIGRID C · 2020 to 2024
$3.7M
Sleep consolidation as a neuroprotective therapy for Alzheimers diseaseR56AG062293 · NIA · UNIVERSITY OF PENNSYLVANIA · PI NAIDOO, NIRMALA NIRINJINI · 2018 to 2018
$403k
NHLBI NIH HHS T32 HL007953NIA NIH HHS R01 AG064231NIA NIH HHS R56 AG062293
6 · The paper itself

Abstract

Many neurodegenerative diseases manifest in an overall aged population, the pathology of which is hallmarked by abnormal protein aggregation. It is known that across aging, sleep quality becomes less efficient and protein homeostatic regulatory mechanisms deteriorate. There is a known relationship between extended wakefulness and poorly consolidated sleep and an increase in cellular stress. In an aged population, when sleep is chronically poor, and proteostatic regulatory mechanisms are less efficient, the cell is inundated with misfolded proteins and suffers a collapse in homeostasis. In this review article, we explore the interplay between aging, sleep quality, and proteostasis and how these processes are implicated in the development and progression of neurodegenerative diseases like Alzheimer's disease (AD). We also present data suggesting that reducing cellular stress and improving proteostasis and sleep quality could serve as potential therapeutic solutions for the prevention or delay in the progression of these diseases.

Indexed as

agingneurodegenarative diseaseproteostasis cell stress and agingsleepunfolded protein response

Identifiers

PMID31244649
PMCPMC6579877
OpenAlexW2951139281

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.