Evidence map›Paper›PMID 39788088›Full record

ReviewNeuron2025

DNA damage and its links to neuronal aging and degeneration.

Ilse Delint-Ramirez, Ram Madabhushi

Abstract readReview
In one paragraph

Review in Neuron, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Article
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  15. Review
  16. 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
  17. Review
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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

2 authors.

Ilse Delint-RamirezDepartments of Psychiatry, Neuroscience, and Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Peter O' Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ram MadabhushiDepartments of Psychiatry, Neuroscience, and Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Peter O' Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: ram.madabhushi@utsouthwestern.edu.

Funding

The impact of stress-induced DNA breaks on chromatin structure, gene activity, and neuron functionR01MH130399 · NIMH · UNIVERSITY OF CINCINNATI · PI Ram Madabhushi, Eric S Wohleb · 2023 to 2026
$3.2M
Mechanisms regulating the formation and repair of neuronal activity-induced DNA breaks in vivo and their effects on chromatin architecture and neuronal physiologyR01MH120132 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI Ram Madabhushi · 2019 to 2026
$3.2M
Regulation of Topoisomerase 2 Beta by phosphorylation at the C-Terminal domainR03MH134200 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI DELINT RAMIREZ, ILSE · 2024 to 2025
$164k
NIMH NIH HHS R01 MH120132NIMH NIH HHS R01 MH130399NIMH NIH HHS R03 MH134200
6 · The paper itself

Abstract

DNA damage is a major risk factor for the decline of neuronal functions with age and in neurodegenerative diseases. While how DNA damage causes neurodegeneration is still being investigated, innovations over the past decade have provided significant insights into this issue. Breakthroughs in next-generation sequencing methods have begun to reveal the characteristics of neuronal DNA damage hotspots and the causes of DNA damage. Chromosome conformation capture-based approaches have shown that, while DNA damage and the ensuing cellular response alter chromatin topology, chromatin organization at damage sites also affects DNA repair outcomes in neurons. Additionally, neuronal activity results in the formation of programmed DNA breaks, which could burden DNA repair mechanisms and promote neuronal dysfunction. Finally, emerging evidence implicates DNA damage-induced inflammation as an important contributor to the age-related decline in neuronal functions. Together, these discoveries have ushered in a new understanding of the significance of genome maintenance for neuronal function.

Indexed as

AgingDNA DamageNeurodegenerative DiseasesNeuronsAnimalsChromatinDNA RepairHumansNerve DegenerationChromatinactive DNA demethylationDNA damagemutationsneurodegenerationneuroinflammationtopoisomerase

Identifiers

PMID39788088
PMCPMC11832075

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.