Evidence map›Paper›PMID 31364066›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019

DNA Damage Repair in Huntington's Disease and Other Neurodegenerative Diseases.

T Maiuri, C E Suart, C L K Hung, K J Graham, C A Barba Bazan, R Truant

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.7field-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

69 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
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  17. Microglia-derived extracellular vesicles trigger age-related neurodegeneration upon DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Review
  19. Review
  20. Review

9 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

6 authors at 1 institution in 1 country.

T MaiuriDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada.
C E SuartDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada.
C L K HungDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada.
K J GrahamDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada.
C A Barba BazanDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada.
R TruantDepartment of Biochemistry and Biomedical Sciences, McMaster University, HSC 4N54, 1200 Main Street West, Hamilton, Ontario, L8N3Z5, Canada. Truantr@mcmaster.ca.ORCID http://orcid.org/0000-0003-2542-6641
McMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent genome-wide association studies of Huntington's disease (HD) primarily highlighted genes involved in DNA damage repair mechanisms as modifiers of age at onset and disease severity, consistent with evidence that more DNA repair genes are being implicated in late age-onset neurodegenerative diseases. This provides an exciting opportunity to advance therapeutic development in HD, as these pathways have already been under intense investigation in cancer research. Also emerging are the roles of other polyglutamine disease proteins in DNA damage repair mechanisms. A potential universal trigger of oxidative DNA damage shared in these late age-onset diseases is the increase of reactive oxygen species (ROS) in human aging, defining an age-related mechanism that has defied other hypotheses of neurodegeneration. We discuss the potential commonality of DNA damage repair pathways in HD and other neurodegenerative diseases. Potential targets for therapy that may prove beneficial across many of these diseases are also identified, defining nodes in the ataxia telangiectasia-mutated (ATM) complex, mismatch repair, and poly ADP-ribose polymerases (PARPs).

Indexed as

AnimalsDNA DamageDNA RepairHumansHuntington DiseaseNeurodegenerative DiseasesOxidative StressPolymorphism, Single NucleotideAtaxia telangiectasia-mutated (ATM)DNA repairHuntington’s diseaseOxidative stressPoly ADP-ribose polymerase (PARP)Spinocerebellar ataxia

Identifiers

PMID31364066
PMCPMC6985310
OpenAlexW2966113050

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.