Evidence map›Paper›PMID 34627838›Full record

ReviewMechanisms of ageing and development2021

A guide to senolytic intervention in neurodegenerative disease.

Suckwon Lee, Ellen Y Wang, Alexandra B Steinberg, Chaska C Walton, Shankar J Chinta, Julie K Andersen

Open access · greenAbstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  13. Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024
    Review
  14. Mutant androgen receptor induces neurite loss and senescence independently of ARE binding in a neuronal model of SBMA.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
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  17. Ageing in the brain: mechanisms and rejuvenating strategies.Cellular and molecular life sciences : CMLS · 2023
    Review
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  19. Periostin Plasma Levels and Changes on Physical and Cognitive Capacities in Community-Dwelling Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
    Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Suckwon LeeBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.
Ellen Y WangBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.
Alexandra B SteinbergUniversity of Wisconsin Department of Biochemistry, 433 Babcock Drive., Madison, WI, 53706, USA.
Chaska C WaltonBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA. Electronic address: CWalton@buckinstitute.org.
Shankar J ChintaBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA; Touro University California, College of Pharmacy, 1310 Club Dr., Vallejo, CA, 94592, USA. Electronic address: schinta@touro.edu.
Julie K AndersenBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA. Electronic address: jandersen@buckinstitute.org.
Buck Institute for Research on Aging · USUniversity of Wisconsin–Madison · US

Funding

Cellular senescence and Alzheimer's diseaseRF1AG068296 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI ANDERSEN, JULIE KAY · 2020 to 2020
$1.9M
NIA NIH HHS RF1 AG068296
6 · The paper itself

Abstract

Cellular senescence is a potential tumor-suppressive mechanism that generally results in an irreversible cell cycle arrest. Senescent cells accumulate with age and actively secrete soluble factors, collectively termed the 'senescence-associated secretory phenotype' (SASP), which has both beneficial and detrimental effects. Although the contribution of senescent cells to age-related pathologies has been well-established outside the brain, emerging evidence indicates that brain cells also undergo cellular senescence and contribute to neuronal loss in the context of age-related neurodegenerative diseases. Contribution of senescent cells in the pathogenesis of neurological disorders has led to the possibility of eliminating senescence cells via pharmacological compounds called senolytics. Recently several senolytics have been demonstrated to elicit improved cognitive performance and healthspan in mouse models of neurodegeneration. However, their translation for use in the clinic still holds several potential challenges. This review summarizes available senolytics, their purported mode of action, and possible off-target effects. We also discuss possible alternative strategies that may help minimize potential side-effects associated with the senolytics approach.

Indexed as

AgingCellular SenescenceNeurodegenerative DiseasesAnimalsHumansMiceSenescence-Associated Secretory PhenotypeSenotherapeuticsSenotherapeuticsAgingImmune surveillanceNeurodegenerationNeurodegenerative diseasesSenescenceSenescence-associated secretory phenotypeSenolytic

Identifiers

PMID34627838
PMCPMC8627445
OpenAlexW3206412239

What OpenQuestion holds

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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.