ReviewChromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology2019
DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases.
Review in Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Bioactivated Glucoraphanin Exerts a Potential Protective Effect in an In Vitro Model of Parkinson's Disease: A Transcriptomic Study.International journal of molecular sciences · 2026Article
- Computationally-designed aptamers targeting RAD51-BRCA2 interaction impair homologous recombination and induce synthetic lethality.Nature communications · 2025Article
- Crosstalk between DNA damage and cGAS-STING immune pathway drives neuroinflammation and dopaminergic neurodegeneration in Parkinson's disease.Brain, behavior, and immunity · 2025Article
- DNA Damage Response Regulation Alleviates Neuroinflammation in a Mouse Model of α-Synucleinopathy.Biomolecules · 2025Article
- Signaling Pathways in Oxidative Stress-Induced Neurodegenerative Diseases: A Review of Phytochemical Therapeutic Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Analysis of Molecular Aspects of Periodontitis as a Risk Factor for Neurodegenerative Diseases: A Single-Center 10-Year Retrospective Cohort Study.International journal of molecular sciences · 2025Article
- Review
- Oxidative genomic or genotoxic stress in neurodegeneration: Mechanisms and therapeutic avenues.AIMS neuroscience · 2025Review
- Redox Homeostasis, Gut Microbiota, and Epigenetics in Neurodegenerative Diseases: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Crosstalk between the DNA damage response and cellular senescence drives aging and age-related diseases.Seminars in immunopathology · 2024Review
- Early oxidative stress and DNA damage in Aβ-burdened hippocampal neurons in an Alzheimer's-like transgenic rat model.Communications biology · 2024Article
- The Neglected Sibling: NLRP2 Inflammasome in the Nervous System.Aging and disease · 2024Review
- Polyphenolic Platform Ameliorated Sanshool for Skin Photoprotection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cell-Free DNA As Peripheral Biomarker of Alzheimer's Disease.Aging and disease · 2024Review
- An Overview of UBTF Neuroregression Syndrome.Brain sciences · 2024Review
- The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing.Translational neurodegeneration · 2024Review
- TDP-43 chronic deficiency leads to dysregulation of transposable elements and gene expression by affecting R-loop and 5hmC crosstalk.Cell reports · 2024Article
- Circulating Cell Free DNA and DNA Double-Strand Breakage in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Review
- Article
- Preleukemic Fusion Genes Induced via Ionizing Radiation.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The complexity of neurodegeneration restricts the ability to understand and treat the neurological disorders affecting millions of people worldwide. Therefore, there is an unmet need to develop new and more effective therapeutic strategies to combat these devastating conditions and that will only be achieved with a better understanding of the biological mechanism associated with disease conditions. Recent studies highlight the role of DNA damage, particularly, DNA double-strand breaks (DSBs), in the progression of neuronal loss in a broad spectrum of human neurodegenerative diseases. This is not unexpected because neurons are prone to DNA damage due to their non-proliferative nature and high metabolic activity. However, it is not clear if DSBs is a primary driver of neuronal loss in disease conditions or simply occurs concomitant with disease progression. Here, we provide evidence that supports a critical role of DSBs in the pathogenesis of the neurodegenerative diseases. Among different kinds of DNA damages, DSBs are the most harmful and perilous type of DNA damage and can lead to cell death if left unrepaired or repaired with error. In this review, we explore the current state of knowledge regarding the role of DSBs repair mechanisms in preserving neuronal function and survival and describe how DSBs could drive the molecular mechanisms resulting in neuronal death in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. We also discuss the potential implications of DSBs as a novel therapeutic target and prognostic marker in patients with neurodegenerative conditions.
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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.