ReviewCurrent neuropharmacology2019
Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases.
Review in Current neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 20 citations in OpenAlex.
- DNA Sensing Pathways in Innate Immunity: Implications for Alzheimer's Disease Progression and Therapy.Molecular neurobiology · 2026Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- cGAS Mediates the Inflammatory Responses of Human Microglial Cells to Genotoxic DNA Damage.Inflammation · 2024Article
- Cell-Free DNA As Peripheral Biomarker of Alzheimer's Disease.Aging and disease · 2024Review
- Circulating Cell Free DNA and DNA Double-Strand Breakage in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Review
- Development of an RNase H2 Activity Assay for Clinical Screening.Journal of clinical medicine · 2023Article
- Cytosolic DNA sensors and glial responses to endogenous DNA.Frontiers in immunology · 2023Review
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Mobile circular DNAs regulating memory and communication in CNS neurons.Frontiers in molecular neuroscience · 2023Article
- Infectious origin of Alzheimer's disease: Amyloid beta as a component of brain antimicrobial immunity.PLoS pathogens · 2022Review
- Genes Possessing the Most Frequent DNA DSBs Are Highly Associated with Development and Cancers, and Essentially Overlap with the rDNA-Contacting Genes.International journal of molecular sciences · 2022Article
- Failure of DNA double-strand break repair by tau mediates Alzheimer's disease pathology in vitro.Communications biology · 2022Article
- Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin.Nucleic acids research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eukaryotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombination, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative disorders including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD) and ataxia telangiectasia (A-T).
Indexed as
Identifiers
What OpenQuestion holds
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.