Evidence map›Paper›PMID 27105872›Full record

ReviewMechanisms of ageing and development2017

Genome instability in Alzheimer disease.

Yujun Hou, Hyundong Song, Deborah L Croteau, Mansour Akbari, Vilhelm A Bohr

Open access · greenAbstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.1field-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

61 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Article
  3. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  4. Article
  5. Review
  6. Investigating DNA damage caused by COVID-19 and influenza in post COVID-19.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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.

Yujun HouLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Hyundong SongLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Mansour AkbariCenter for Healthy Aging, SUND, University of Copenhagen, Denmark.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224, 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
NIA Interlab: Mitophagy upregulation as a therapeutic strategy for Alzheimer's diseaseZIAAG000782 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2016 to 2019
$1.5M
Intramural NIH HHS ZIA AG000723
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. Autosomal dominant, familial AD (fAD) is very rare and caused by mutations in amyloid precursor protein (APP), presenilin-1 (PSEN-1), and presenilin-2 (PSEN-2) genes. The pathogenesis of sporadic AD (sAD) is more complex and variants of several genes are associated with an increased lifetime risk of AD. Nuclear and mitochondrial DNA integrity is pivotal during neuronal development, maintenance and function. DNA damage and alterations in cellular DNA repair capacity have been implicated in the aging process and in age-associated neurodegenerative diseases, including AD. These findings are supported by research using animal models of AD and in DNA repair deficient animal models. In recent years, novel mechanisms linking DNA damage to neuronal dysfunction have been identified and have led to the development of noninvasive treatment strategies. Further investigations into the molecular mechanisms connecting DNA damage to AD pathology may help to develop novel treatment strategies for this debilitating disease. Here we provide an overview of the role of genome instability and DNA repair deficiency in AD pathology and discuss research strategies that include genome instability as a component.

Indexed as

Genomic InstabilityMutationAlzheimer DiseaseAmyloid beta-Protein PrecursorDNA DamageDNA RepairHumansNeuronsPresenilin-1Amyloid beta-Protein PrecursorAPP protein, humanPresenilin-1PSEN1 protein, humanAlzheimer’s diseaseDNA damageDNA repair

Identifiers

PMID27105872
PMCPMC5195918
OpenAlexW2342148852

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.