ReviewNeural regeneration research2018
DNA plasticity and damage in amyotrophic lateral sclerosis.
Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled 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.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Gene expression profiles in sporadic ALS fibroblasts define disease subtypes and the metabolic effects of the investigational drug EH301.Human molecular genetics · 2022Pooled it
- ERVK activity in CD8Journal of neuroinflammation · 2026Article
- Extrachromosomal circular DNA: a double-edged sword in cancer progression and age-related diseases.Human cell · 2025Review
- Adenosine diphosphate-ribosylation greatly affects proteins function: a focus on neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Poly ADP-ribose signaling is dysregulated in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Tardigrade damage suppressor protein Dsup promotes DNA damage in neurons.Molecular and cellular neurosciences · 2023Article
- Review
- Predicted Cellular Interactors of the Endogenous Retrovirus-K Integrase Enzyme.Microorganisms · 2021Article
- Differential responses of neurons, astrocytes, and microglia to G-quadruplex stabilization.Aging · 2021Article
- Role and therapeutic potential of liquid-liquid phase separation in amyotrophic lateral sclerosis.Journal of molecular cell biology · 2021Review
- Base Excision Repair AP-Endonucleases-Like Genes Modulate DNA Damage Response and Virulence of the Human PathogenJournal of fungi (Basel, Switzerland) · 2021Article
- Trends in Understanding the Pathological Roles of TDP-43 and FUS Proteins.Advances in experimental medicine and biology · 2021Article
- Locus-specific analysis of Transposable Elements during the progression of ALS in the SOD1G93A mouse model.PloS one · 2021Article
- Frequency and methylation status of selected retrotransposition competent L1 loci in amyotrophic lateral sclerosis.Molecular brain · 2020Article
- Emerging Technologies for Genome-Wide Profiling of DNA Breakage.Frontiers in genetics · 2020Review
- Review
- Ageing as a risk factor for neurodegenerative disease.Nature reviews. Neurology · 2019Review
- VRK1 functional insufficiency due to alterations in protein stability or kinase activity of human VRK1 pathogenic variants implicated in neuromotor syndromes.Scientific reports · 2019Article
- Nuclear Phospho-SOD1 Protects DNA from Oxidative Stress Damage in Amyotrophic Lateral Sclerosis.Journal of clinical medicine · 2019Article
- Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC.Frontiers in neurology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiology of amyotrophic lateral sclerosis (ALS) is particularly challenging due to the heterogeneity of its clinical presentation and the diversity of cellular, molecular and genetic peculiarities involved. Molecular insights unveiled several novel genetic factors to be inherent in both familial and sporadic disease entities, whose characterizations in terms of phenotype prediction, pathophysiological impact and putative prognostic value are a topic of current researches. However, apart from genetically well-defined high-confidence and other susceptibility loci, the role of DNA damage and repair strategies of the genome as a whole, either elicited as a direct consequence of the underlying genetic mutation or seen as an autonomous parameter, in the initiation and progression of ALS, and the different cues involved in either process are still incompletely understood. This mini review summarizes current knowledge on DNA alterations and counteracting DNA repair strategies in ALS pathology and discusses the putative role of unconventional DNA entities including transposable elements and extrachromosomal circular DNA in the disease process. Focus is set on SOD1-related pathophysiology, with extension to FUS, TDP-43 and C9ORF72 mutations. Advancing our knowledge in the field will contribute to an improved understanding of this relentless disease, for which therapeutic options others than symptomatic approaches are almost unavailable.
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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.