Evidence map›Paper›PMID 30261683›Full record

ReviewInternational journal of molecular sciences2018

Ageing, Cellular Senescence and Neurodegenerative Disease.

Marios Kritsilis, Sophia V Rizou, Paraskevi N Koutsoudaki, Konstantinos Evangelou, Vassilis G Gorgoulis, Dimitrios Papadopoulos

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed, 6 pooled it
17.8field-weighted citation impact, top 1% 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

239 citing papers in PubMed, 6 syntheses or guidelines pooled it, 427 citations in OpenAlex.

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  13. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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179 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

6 authors at 1 institution in 1 country.

Marios KritsilisLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. marios.kritsilis@gmail.com.
Sophia V RizouLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. sofiriz92@gmail.com.
Paraskevi N KoutsoudakiLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. pkoutsoudaki@med.uoa.gr.
Konstantinos EvangelouLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. cnevagel@med.uoa.gr.
Vassilis G GorgoulisLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. vgorg@med.uoa.gr.
Dimitrios PapadopoulosLaboratory of Histology & Embryology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 115-27 Athens, Greece. d.papadopoulos@otenet.gr.
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ageing is a major risk factor for developing many neurodegenerative diseases. Cellular senescence is a homeostatic biological process that has a key role in driving ageing. There is evidence that senescent cells accumulate in the nervous system with ageing and neurodegenerative disease and may predispose a person to the appearance of a neurodegenerative condition or may aggravate its course. Research into senescence has long been hindered by its variable and cell-type specific features and the lack of a universal marker to unequivocally detect senescent cells. Recent advances in senescence markers and genetically modified animal models have boosted our knowledge on the role of cellular senescence in ageing and age-related disease. The aim now is to fully elucidate its role in neurodegeneration in order to efficiently and safely exploit cellular senescence as a therapeutic target. Here, we review evidence of cellular senescence in neurons and glial cells and we discuss its putative role in Alzheimer's disease, Parkinson's disease and multiple sclerosis and we provide, for the first time, evidence of senescence in neurons and glia in multiple sclerosis, using the novel GL13 lipofuscin stain as a marker of cellular senescence.

Indexed as

Cellular SenescenceAgingAnimalsHumansNeurodegenerative DiseasesageingAlzheimer’s diseasecellular senescencelipofuscinmultiple sclerosisneurodegenerationParkinson’s diseasesenolyticsSenTraGorTM (GL13)

Identifiers

PMID30261683
PMCPMC6213570
OpenAlexW2892390537

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.