Evidence map›Paper›PMID 18701195›Full record

ArticleNeurobiology of aging2010

Differential age-related changes in mitochondrial DNA repair activities in mouse brain regions.

Ricardo Gredilla, Christian Garm, Rikke Holm, Vilhelm A Bohr, Tinna Stevnsner

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  13. Mitochondrial DNA deletions in Alzheimer's brains: a review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014
    Review
  14. Article
  15. Oxidative stress and pulmonary fibrosis.Biochimica et biophysica acta · 2013
    Review
  16. Review
  17. Review
  18. Review
  19. Minimizing the damage: repair pathways keep mitochondrial DNA intact.Nature reviews. Molecular cell biology · 2012
    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

5 authors at 2 institutions in 2 countries.

Ricardo GredillaDanish Center of Molecular Gerontology, University of Aarhus, Department of Molecular Biology, Aarhus C, Denmark.
Christian Garm
Rikke Holm
Vilhelm A Bohr
Tinna Stevnsner
Aarhus University · DKNational Institutes of Health · 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 STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
Intramural NIH HHS Z01 AG000733
6 · The paper itself

Abstract

Aging in the brain is characterized by increased susceptibility to neuronal loss and functional decline, and mitochondrial DNA (mtDNA) mutations are thought to play an important role in these processes. Due to the proximity of mtDNA to the main sites of mitochondrial free radical generation, oxidative stress is a major source of DNA mutations in mitochondria. The base excision repair (BER) pathway removes oxidative lesions from mtDNA, thereby constituting an important mechanism to avoid accumulation of mtDNA mutations. The complexity of the brain implies that exposure and defence against oxidative stress varies among brain regions and hence some regions may be particularly prone to accumulation of mtDNA damages. In the current study we investigated the efficiency of the BER pathway throughout the murine lifespan in mitochondria from cortex and hippocampus, regions that are central in mammalian cognition, and which are severely affected during aging and in neurodegenerative diseases. A regional specific regulation of mitochondrial DNA repair activities was observed with aging. In cortical mitochondria, DNA glycosylase activities peaked at middle-age followed by a significant drop at old age. However, only minor changes were observed in hippocampal mitochondria during the whole lifespan of the animals. Furthermore, DNA glycosylase activities were lower in hippocampal than in cortical mitochondria. Mitochondrial AP endonuclease activity increased in old animals in both brain regions. Our data suggest an important regional specific regulation of mitochondrial BER during aging.

Indexed as

AgingAnimalsBrainDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA, MitochondrialDNA RepairLamin Type BMaleMiceMice, Inbred C57BLMitochondrial ProteinsSpinal CordVoltage-Dependent Anion Channel 1DNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA, MitochondrialLamin Type BMitochondrial ProteinsNeil1 protein, mouseOgg1 protein, mouseVoltage-Dependent Anion Channel 1

Identifiers

PMID18701195
PMCPMC2858237
OpenAlexW2066323090

What OpenQuestion holds

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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.