Evidence map›Paper›PMID 18378358›Full record

ArticleNeurobiology of aging2009

DNA base excision repair activities in mouse models of Alzheimer's disease.

Lior Weissman, Nadja C de Souza-Pinto, Mark P Mattson, Vilhelm A Bohr

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Genome instability in Alzheimer disease.Mechanisms of ageing and development · 2017
    Review
  7. Article
  8. Genomic integrity and the ageing brain.Nature reviews. Neuroscience · 2015
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. DNA repair deficiency in neurodegeneration.Progress in neurobiology · 2011
    Review
  18. 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

4 authors at 2 institutions in 1 country.

Lior WeissmanLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
Nadja C de Souza-Pinto
Mark P Mattson
Vilhelm A Bohr
National Institute on Aging · USNational Institutes of Health · US

Funding

Function of RecQ helicases in genome stabilityZIAAG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$13.1M
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
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Apoptosis In Neurodegenerative DisordersZIAAG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Function of RecQ helicases in genome stabilityZ01AG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1993 to 2008
$2.9M
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
REPAIR OF OXIDATIVE DNA DAMAGEZ01AG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1994 to 2008
$1.3M
PROCESSING OF OXIDATIVE STRESS IN ALZHEIMER'S DISEASEZ01AG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1997 to 2008
$565k
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 AG000726Intramural NIH HHS Z01 AG000727Intramural NIH HHS Z01 AG000733Intramural NIH HHS Z01 AG000735
6 · The paper itself

Abstract

Alzheimer's disease (AD) has been correlated with elevated levels of oxidative DNA damage. Base excision repair (BER) is the main repair pathway for the removal of oxidative DNA base modifications. We have recently found significant functional deficiencies in BER in brains of sporadic AD and amnestic mild cognitive impairment patients. In this study we tested whether altered BER activities are associated with appearance of symptoms in different brain regions of pre-symptomatic and symptomatic mice harboring mutant APP alone or in combination with Tau and PS1. Our results suggest that unlike in humans, the development of AD-like pathology in the studied mouse models is not associated with deficiencies in BER.

Indexed as

DNADNA RepairAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, TransgenicMutationPresenilin-1Protease NexinsReceptors, Cell SurfaceAmyloid beta-Protein PrecursorAPP protein, humanDNAMAPT protein, humanPresenilin-1Protease NexinsPSEN1 protein, humanReceptors, Cell Surfacetau Proteins

Identifiers

PMID18378358
PMCPMC2763940
OpenAlexW2068803114

What OpenQuestion holds

Textmetadata
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.