Evidence map›Paper›PMID 23643943›Full record

ArticleMechanisms of ageing and development2013

Base excision repair in the mammalian brain: implication for age related neurodegeneration.

Peter Sykora, David M Wilson, Vilhelm A Bohr

Open access · greenAbstract read
In one paragraph

Article in Mechanisms of ageing and development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  11. Diagnostics (Basel, Switzerland) · 2020
    Article
  12. Apurinic endonuclease-1 preserves neural genome integrity to maintain homeostasis and thermoregulation and prevent brain tumors.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. Review
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  19. Genome instability in Alzheimer disease.Mechanisms of ageing and development · 2017
    Review
  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

3 authors at 1 institution in 1 country.

Peter SykoraLaboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, United States.
David M Wilson
Vilhelm A Bohr
National Institute on Aging · US

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
Oxidative DNA Damage Repair in Premature Aging and NeurodegenerationZIAAG000751 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.3M
GROWTH ARREST AND DNA DAMAGE INDUCIBLE GENE GADD153--REGULATION BY DNA DAMAGEZ01AG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM · 1992 to 2008
$310k
Intramural NIH HHS Z01 AG000723
6 · The paper itself

Abstract

The repair of damaged DNA is essential to maintain longevity of an organism. The brain is a matrix of different neural cell types including proliferative astrocytes and post-mitotic neurons. Post-mitotic DNA repair is a version of proliferative DNA repair, with a reduced number of available pathways and most of these attenuated. Base excision repair (BER) is one pathway that remains robust in neurons; it is this pathway that resolves the damage due to oxidative stress. This oxidative damage is an unavoidable byproduct of respiration, and considering the high metabolic activity of neurons this type of damage is particularly pertinent in the brain. The accumulation of oxidative DNA damage over time is a central aspect of the theory of aging and repair of such chronic damage is of the highest importance. We review research conducted in BER mouse models to clarify the role of this pathway in the neural system. The requirement for BER in proliferating cells also correlates with high levels of many of the BER enzymes in neurogenesis after DNA damage. However, the pathway is also necessary for normal neural maintenance as larger infarct volumes after ischemic stroke are seen in some glycosylase deficient animals. Further, the requirement for DNA polymerase β in post-mitotic BER is potentially more important than in proliferating cells due to reduced levels of replicative polymerases. The BER response may have particular relevance for the onset and progression of many neurodegenerative diseases associated with an increase in oxidative stress including Alzheimer's.

Indexed as

DNA DamageDNA RepairAgingAnimalsBrainBrain IschemiaDisease Models, AnimalMiceNeurodegenerative DiseasesNeuronsRatsStrokeAgingBERDNA repairNeurodegeneration

Identifiers

PMID23643943
PMCPMC3834072
OpenAlexW1983496878

What OpenQuestion holds

Textmetadata
LicenceTDM
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.