Evidence map›Paper›PMID 25128619›Full record

ReviewJournal of molecular biology2014

Chromatin regulation of DNA damage repair and genome integrity in the central nervous system.

Ling Pan, Jay Penney, Li-Huei Tsai

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Compound HeterozygousNeuroSci · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Ling PanPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Jay PenneyPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Li-Huei TsaiPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: lhtsai@mit.edu.
Massachusetts Institute of Technology · US

Funding

Targeting a Novel Regulator of Brain Aging and Alzheimer's Disease (ADMINISTRATIVE SUPPLEMENT- SAGE)R01AG046174 · NIA · HARVARD MEDICAL SCHOOL · PI TSAI, LI-HUEI, YANKNER, BRUCE A · 2014 to 2018
$4.9M
NIA NIH HHS R01 AG046174
6 · The paper itself

Abstract

With the continued extension of lifespan, aging and age-related diseases have become a major medical challenge to our society. Aging is accompanied by changes in multiple systems. Among these, the aging process in the central nervous system is critically important but very poorly understood. Neurons, as post-mitotic cells, are devoid of replicative associated aging processes, such as senescence and telomere shortening. However, because of the inability to self-replenish, neurons have to withstand challenge from numerous stressors over their lifetime. Many of these stressors can lead to damage of the neurons' DNA. When the accumulation of DNA damage exceeds a neuron's capacity for repair, or when there are deficiencies in DNA repair machinery, genome instability can manifest. The increased mutation load associated with genome instability can lead to neuronal dysfunction and ultimately to neuron degeneration. In this review, we first briefly introduce the sources and types of DNA damage and the relevant repair pathways in the nervous system (summarized in Fig. 1). We then discuss the chromatin regulation of these processes and summarize our understanding of the contribution of genomic instability to neurodegenerative diseases.

Indexed as

DNA DamageCentral Nervous SystemChromatinDNA RepairGenomic InstabilityHumansModels, GeneticMutationNeurodegenerative DiseasesNeuronsChromatincentral nervous systemDNA damage responseDNA repairhistone modificationsneurodegenerative diseases

Identifiers

PMID25128619
PMCPMC5560486
OpenAlexW2079658347

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.