Evidence map›Paper›PMID 37055865›Full record

ReviewTranslational neurodegeneration2023

Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.

Sina Shadfar, Sonam Parakh, Md Shafi Jamali, Julie D Atkin

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
17.4field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Neuroprotective properties ofIBRO neuroscience reports · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Methods to Study DNA Damage Using Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  17. Article
  18. Cystathionine γ-lyase is a major regulator of cognitive function through neurotrophin signaling and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Hemocyanin controlsVirulence · 2025
    Article

17 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

4 authors at 2 institutions in 1 country.

Sina ShadfarCentre for Motor Neuron Disease Research, Macquarie Medical School, Macquarie University, Sydney, NSW, 2109, Australia. sina.shadfar@mq.edu.au.ORCID 0000-0001-7626-1096
Sonam ParakhCentre for Motor Neuron Disease Research, Macquarie Medical School, Macquarie University, Sydney, NSW, 2109, Australia.ORCID 0000-0002-7048-9695
Md Shafi JamaliCentre for Motor Neuron Disease Research, Macquarie Medical School, Macquarie University, Sydney, NSW, 2109, Australia.ORCID 0000-0001-5108-2286
Julie D AtkinCentre for Motor Neuron Disease Research, Macquarie Medical School, Macquarie University, Sydney, NSW, 2109, Australia. Julie.atkin@mq.edu.au.ORCID 0000-0003-2427-499X
Macquarie University · AULa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Redox homeostasis refers to the balance between the production of reactive oxygen species (ROS) as well as reactive nitrogen species (RNS), and their elimination by antioxidants. It is linked to all important cellular activities and oxidative stress is a result of imbalance between pro-oxidants and antioxidant species. Oxidative stress perturbs many cellular activities, including processes that maintain the integrity of DNA. Nucleic acids are highly reactive and therefore particularly susceptible to damage. The DNA damage response detects and repairs these DNA lesions. Efficient DNA repair processes are therefore essential for maintaining cellular viability, but they decline considerably during aging. DNA damage and deficiencies in DNA repair are increasingly described in age-related neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and Huntington's disease. Furthermore, oxidative stress has long been associated with these conditions. Moreover, both redox dysregulation and DNA damage increase significantly during aging, which is the biggest risk factor for neurodegenerative diseases. However, the links between redox dysfunction and DNA damage, and their joint contributions to pathophysiology in these conditions, are only just emerging. This review will discuss these associations and address the increasing evidence for redox dysregulation as an important and major source of DNA damage in neurodegenerative disorders. Understanding these connections may facilitate a better understanding of disease mechanisms, and ultimately lead to the design of better therapeutic strategies based on preventing both redox dysregulation and DNA damage.

Indexed as

Neurodegenerative DiseasesAntioxidantsDNA DamageHumansOxidation-ReductionOxidative StressReactive Oxygen SpeciesAntioxidantsReactive Oxygen SpeciesDNA damageNeurodegenerationOxidative stressReactive oxygen speciesRedox dysregulation

Identifiers

PMID37055865
PMCPMC10103468
OpenAlexW4365482594

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.