Evidence map›Paper›PMID 20708822›Full record

ArticleNeurobiology of aging2012

Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease.

Ricardo Gredilla, Lior Weissman, Jenq-Lin Yang, Vilhelm A Bohr, Tinna Stevnsner

Abstract read
In one paragraph

Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Mitochondrial DNA deletions in Alzheimer's brains: a review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Neurodegeneration as an RNA disorder.Progress in neurobiology · 2012
    Review
  15. Review
  16. Article
  17. DNA repair deficiency in neurodegeneration.Progress in neurobiology · 2011
    Review
  18. Review
  19. 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

5 authors at 2 institutions in 2 countries.

Ricardo GredillaDanish Center for Molecular Gerontology, Department of Molecular Biology, University of Aarhus, Aarhus, Denmark.
Lior Weissman
Jenq-Lin Yang
Vilhelm A Bohr
Tinna Stevnsner
National Institute on Aging · USAarhus University · 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
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
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 AG000723Intramural NIH HHS Z01 AG000733Intramural NIH HHS ZIA AG000735
6 · The paper itself

Abstract

Brain aging is associated with synaptic decline and synaptic function is highly dependent on mitochondria. Increased levels of oxidative DNA base damage and accumulation of mitochondrial DNA (mtDNA) mutations or deletions lead to mitochondrial dysfunction, playing an important role in the aging process and the pathogenesis of several neurodegenerative diseases. Here we have investigated the repair of oxidative base damage, in synaptosomes of mouse brain during normal aging and in an AD model. During normal aging, a reduction in the base excision repair (BER) capacity was observed in the synaptosomal fraction, which was associated with a decrease in the level of BER proteins. However, we did not observe changes between the synaptosomal BER activities of presymptomatic and symptomatic AD mice harboring mutated amyolid precursor protein (APP), Tau, and presinilin-1 (PS1) (3xTgAD). Our findings suggest that the age-related reduction in BER capacity in the synaptosomal fraction might contribute to mitochondrial and synaptic dysfunction during aging. The development of AD-like pathology in the 3xTgAD mouse model was, however, not associated with deficiencies of the BER mechanisms in the synaptosomal fraction when the whole brain was analyzed.

Indexed as

DNA, MitochondrialDNA RepairAge FactorsAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalDNA DamageDNA GlycosylasesHumansLamin Type AMaleMiceMice, TransgenicAmyloid beta-Protein PrecursorDNA GlycosylasesDNA, MitochondrialLamin Type APresenilin-1PSEN1 protein, humantau ProteinsVdac1 protein, mouseVoltage-Dependent Anion Channel 1

Identifiers

PMID20708822
PMCPMC3041866
OpenAlexW2078242847

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.