ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2013
Chromatin modifications associated with DNA double-strand breaks repair as potential targets for neurological diseases.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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.
Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- DNA Damage and Chromatin Rearrangement Work Together to Promote Neurodegeneration.Molecular neurobiology · 2025Review
- Investigation into the Neuroprotective and Therapeutic Potential of Plant-Derived Chk2 Inhibitors.International journal of molecular sciences · 2024Review
- Sulforaphane and Its Protective Role in Prostate Cancer: A Mechanistic Approach.International journal of molecular sciences · 2023Review
- Inhibition of Chk2 promotes neuroprotection, axon regeneration, and functional recovery after CNS injury.Science advances · 2022Article
- The brain-penetrant ATM inhibitor, AZD1390, promotes axon regeneration and functional recovery in preclinical models of spinal cord injury.Clinical and translational medicine · 2022Article
- The Role of the Natural Antioxidant Mechanism in Sperm Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- Failure of DNA double-strand break repair by tau mediates Alzheimer's disease pathology in vitro.Communications biology · 2022Article
- Tricyclodecan-9-yl-Xanthogenate (D609): Mechanism of Action and Pharmacological Applications.International journal of molecular sciences · 2022Review
- DNA Damage-Induced Neurodegeneration in Accelerated Ageing and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Molecular Mechanisms of Specific Cellular DNA Damage Response and Repair Induced by the Mixed Radiation Field During Boron Neutron Capture Therapy.Frontiers in oncology · 2021Review
- Possible Epigenetic Role of Vitexin in Regulating Neuroinflammation in Alzheimer's Disease.Journal of immunology research · 2020Review
- 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 · 2019Review
- Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases.Current neuropharmacology · 2019Review
- Extracellular vesicles as trans-genomic agents: Emerging roles in disease and evolution.Cancer science · 2017Review
- NRAGE is involved in homologous recombination repair to resist the DNA-damaging chemotherapy and composes a ternary complex with RNF8-BARD1 to promote cell survival in squamous esophageal tumorigenesis.Cell death and differentiation · 2016Article
- Poly(ADP-ribose) polymerase 1 is a novel target to promote axonal regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Prion-induced neurotoxicity: Possible role for cell cycle activity and DNA damage response.World journal of virology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. Neurons, due to their post-mitotic state, high metabolism, and longevity are particularly prone to the accumulation of DNA lesions. Indeed, DNA damage has been suggested as a major contributor to both age-associated neurodegenerative diseases and acute neurological injury. The DNA damage response is a key factor in maintaining genome integrity. It relies on highly dynamic posttranslational modifications of the chromatin and DNA repair proteins to allow signaling, access, and repair of the lesion. Drugs that modulate the activity of the enzymes responsible for these modifications have emerged as attractive therapeutic compounds to treat neurodegeneration. In this review, we discuss the role of DNA double-strand breaks and abnormal chromatin modification patterns in a range of neurodegenerative conditions, and the chromatin modifiers that might ameliorate them. Finally, we suggest that understanding the epigenetic modifications specific to neuronal DNA repair is crucial for the development of efficient neurotherapeutic strategies.
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Registered trials
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.