Evidence map›Paper›PMID 38076538›Full record

ReviewFrontiers in aging neuroscience2023

Cellular senescence in brain aging and cognitive decline.

Areez Shafqat, Saifullah Khan, Mohamed H Omer, Mahnoor Niaz, Ibrahem Albalkhi, Khaled AlKattan, Ahmed Yaqinuddin, Tamara Tchkonia, James L Kirkland, Shahrukh K Hashmi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.9field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

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  12. The Yin-Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2026
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  18. Integrated transcriptomic profiling combined withFrontiers in aging neuroscience · 2026
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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

10 authors at 5 institutions in 5 countries.

Areez Shafqat *College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Saifullah Khan *Medical College, Aga Khan University, Karachi, Pakistan.
Mohamed H OmerSchool of Medicine, Cardiff University, Cardiff, United Kingdom.
Mahnoor NiazMedical College, Aga Khan University, Karachi, Pakistan.
Ibrahem AlbalkhiCollege of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Khaled AlKattanCollege of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Ahmed YaqinuddinCollege of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, United States.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, United States.
Shahrukh K HashmiDepartment of Internal Medicine, Mayo Clinic, Rochester, MN, United States.
Alfaisal University · SAAga Khan University · PKMayo Clinic in Florida · USCardiff University · GBKhalifa University of Science and Technology · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a biological aging hallmark that plays a key role in the development of neurodegenerative diseases. Clinical trials are currently underway to evaluate the effectiveness of senotherapies for these diseases. However, the impact of senescence on brain aging and cognitive decline in the absence of neurodegeneration remains uncertain. Moreover, patient populations like cancer survivors, traumatic brain injury survivors, obese individuals, obstructive sleep apnea patients, and chronic kidney disease patients can suffer age-related brain changes like cognitive decline prematurely, suggesting that they may suffer accelerated senescence in the brain. Understanding the role of senescence in neurocognitive deficits linked to these conditions is crucial, especially considering the rapidly evolving field of senotherapeutics. Such treatments could help alleviate early brain aging in these patients, significantly reducing patient morbidity and healthcare costs. This review provides a translational perspective on how cellular senescence plays a role in brain aging and age-related cognitive decline. We also discuss important caveats surrounding mainstream senotherapies like senolytics and senomorphics, and present emerging evidence of hyperbaric oxygen therapy and immune-directed therapies as viable modalities for reducing senescent cell burden.

Indexed as

agingastrocyte senescencecellular senescencecognitive declinemicroglia senescenceobesitytherapy-induced senescence (TIS)traumatic brain injury

Identifiers

PMID38076538
PMCPMC10702235
OpenAlexW4388945505

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.