Evidence map›Paper›PMID 30472697›Full record

ArticleAging2018

Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging.

Quratul Ain, Christian Schmeer, Diane Penndorf, Mike Fischer, Tzvetanka Bondeva, Martin Förster, Ronny Haenold, Otto W Witte, Alexandra Kretz

Open access · greenAbstract read
In one paragraph

Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Nutrition Interventions of Herbal Compounds on Cellular Senescence.Oxidative medicine and cellular longevity · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Molecular and cellular pathways contributing to brain aging.Behavioral and brain functions : BBF · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

Quratul Ain *Hans Berger Department of Neurology, Jena University Hospital, Jena, Thuringia 07747, Germany.
Christian Schmeer *Hans Berger Department of Neurology, Jena University Hospital, Jena, Thuringia 07747, Germany.
Diane PenndorfHans Berger Department of Neurology, Jena University Hospital, Jena, Thuringia 07747, Germany.
Mike FischerDepartment of Internal Medicine II, Jena University Hospital, Jena, Thuringia 07747, Germany.
Tzvetanka BondevaDepartment of Internal Medicine III, Jena University Hospital, Jena, Thuringia 07747, Germany.
Martin FörsterDepartment of Internal Medicine I, Jena University Hospital, Jena, Thuringia 07747, Germany.
Ronny HaenoldLeibniz Institute on Aging - Fritz Lipmann Institute, 07745 Jena, Thuringia, Germany.
Otto W WitteHans Berger Department of Neurology, Jena University Hospital, Jena, Thuringia 07747, Germany.
Alexandra KretzHans Berger Department of Neurology, Jena University Hospital, Jena, Thuringia 07747, Germany.
Jena University Hospital · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replication-based telomere shortening during lifetime is species- and tissue-specific, however, its impact on healthy aging is unclear. In particular, the contribution of telomere truncation to the aging process of the CNS, where replicative senescence alone fails to explain organ aging due to low to absent mitotic activity of intrinsic populations, is undefined. Here, we assessed changes in relative telomere length in non-replicative and replicative neural brain populations and telomerase activity as a function of aging in C57BL/6 mice. Telomeres in neural cells and sub-selected neurons shortened with aging in a cell cycle-dependent and -independent manner, with preponderance in replicative moieties, implying that proliferation accelerates, but is not prerequisite for telomere shortening. Consistent with this telomere erosion, telomerase activity and nuclear TERT protein were not induced with aging. Knockdown of the

Indexed as

AgingAnimalsCell CycleCerebral CortexMiceNeuronsTelomeraseTelomere ShorteningTranscription Factor RelARela protein, mouseTelomeraseTert protein, mouseTranscription Factor RelAbrain agingcell cyclecellular senescenceRelA subunit of nuclear factor kappa Btelomerase reverse transcriptasetelomere length

Identifiers

PMID30472697
PMCPMC6286833
OpenAlexW2900987624

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.