Evidence map›Paper›PMID 26002197›Full record

ReviewDNA repair2015

The role of DNA base excision repair in brain homeostasis and disease.

Mansour Akbari, Marya Morevati, Deborah Croteau, Vilhelm A Bohr

Abstract readReview
In one paragraph

Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Contributions of DNA Damage to Alzheimer's Disease.International journal of molecular sciences · 2020
    Review
  10. Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019
    Article
  11. Review
  12. Article
  13. 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
  14. Article
  15. Review
  16. Base excision repair of oxidative DNA damage: from mechanism to disease.Frontiers in bioscience (Landmark edition) · 2017
    Review
  17. Review
  18. Article
  19. 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

4 authors at 2 institutions in 2 countries.

Mansour AkbariCenter for Healthy Aging, SUND, University of Copenhagen, Denmark.
Marya MorevatiCenter for Healthy Aging, SUND, University of Copenhagen, Denmark.
Deborah CroteauLaboratory of Molecular Gerontology, National Institute on Aging, 251 Bayview Blvd, Baltimore, USA.
Vilhelm A BohrCenter for Healthy Aging, SUND, University of Copenhagen, Denmark; Laboratory of Molecular Gerontology, National Institute on Aging, 251 Bayview Blvd, Baltimore, USA. Electronic address: vbohr@nih.gov.
National Institute on Aging · USUniversity of Copenhagen · DK

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Processing Of Oxidative Stress In AlzheimerZIAAG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.4M
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
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

Chemical modification and spontaneous loss of nucleotide bases from DNA are estimated to occur at the rate of thousands per human cell per day. DNA base excision repair (BER) is a critical mechanism for repairing such lesions in nuclear and mitochondrial DNA. Defective expression or function of proteins required for BER or proteins that regulate BER have been consistently associated with neurological dysfunction and disease in humans. Recent studies suggest that DNA lesions in the nuclear and mitochondrial compartments and the cellular response to those lesions have a profound effect on cellular energy homeostasis, mitochondrial function and cellular bioenergetics, with especially strong influence on neurological function. Further studies in this area could lead to novel approaches to prevent and treat human neurodegenerative disease.

Indexed as

DNA RepairBrainDNA DamageDNA HelicasesDNA, MitochondrialDNA Repair EnzymesGene Expression RegulationHomeostasisHumansMitochondriaNeurodegenerative DiseasesOxidative StressPhosphotransferases (Alcohol Group Acceptor)Poly-ADP-Ribose Binding ProteinsPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesDNA HelicasesDNA, MitochondrialDNA Repair EnzymesERCC6 protein, humanPARP1 protein, humanPhosphotransferases (Alcohol Group Acceptor)PNKP protein, humanPoly-ADP-Ribose Binding ProteinsPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesBase excision repairMitochondrial DNANeurodegenerationOxidative damagePARP-1

Identifiers

PMID26002197
PMCPMC5576892
OpenAlexW2085040893

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.