ArticleCell reports2021
Base excision repair causes age-dependent accumulation of single-stranded DNA breaks that contribute to Parkinson disease pathology.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 46 citations in OpenAlex.
- Functional impact of Nth like DNA glycosylase 1 on mitochondrial dynamics.Nucleic acids research · 2026Article
- Hypomorphic Protein Expression of DNA Polymerase Beta in PolβBiomolecules · 2026Article
- Role of Microglial Dysfunction in Parkinson's Disease: From Multifactorial Causes to Neurodegeneration.Neuroscience bulletin · 2026Review
- Adjunctive EGb 761 treatment in patients with Parkinson's disease: a case series.Frontiers in aging neuroscience · 2026Article
- Shared molecular mechanisms in aging and neurodegenerative diseases: from mechanistic insights to therapeutic strategies.Frontiers in human neuroscience · 2026Review
- Repair and regeneration across the lifespan: an ontogenetic perspective.Frontiers in aging · 2026Review
- Review
- Longitudinal assessment of DNA repair signature trajectory in prodromal versus established Parkinson's disease.NPJ Parkinson's disease · 2025Article
- The chromatin regulator HELLS mediates SSB repair and responses to DNA alkylation damage.Nucleic acids research · 2025Article
- Emerging strategies, applications and challenges of targeting NADNature aging · 2025Review
- Utilization of natural products in diverse pathogeneses of diseases associated with single or double DNA strand damage repair.Chinese medicine · 2025Review
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025Review
- Super-resolution imaging reveals nucleolar encapsulation by single-stranded DNA.Journal of cell science · 2024Article
- Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.Nucleic acids research · 2024Article
- Single-cell analysis reveals the disparities in immune profiles between younger and elder patients.European geriatric medicine · 2024Article
- Review
- Article
- Recent advances and current challenges of new approach methodologies in developmental and adult neurotoxicity testing.Archives of toxicology · 2024Review
- Spatial transcriptomics reveals molecular dysfunction associated with cortical Lewy pathology.Nature communications · 2024Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging, genomic stress, and mitochondrial dysfunction are risk factors for neurodegenerative pathologies, such as Parkinson disease (PD). Although genomic instability is associated with aging and mitochondrial impairment, the underlying mechanisms are poorly understood. Here, we show that base excision repair generates genomic stress, promoting age-related neurodegeneration in a Caenorhabditis elegans PD model. A physiological level of NTH-1 DNA glycosylase mediates mitochondrial and nuclear genomic instability, which promote degeneration of dopaminergic neurons in older nematodes. Conversely, NTH-1 deficiency protects against α-synuclein-induced neurotoxicity, maintaining neuronal function with age. This apparent paradox is caused by modulation of mitochondrial transcription in NTH-1-deficient cells, and this modulation activates LMD-3, JNK-1, and SKN-1 and induces mitohormesis. The dependance of neuroprotection on mitochondrial transcription highlights the integration of BER and transcription regulation during physiological aging. Finally, whole-exome sequencing of genomic DNA from patients with idiopathic PD suggests that base excision repair might modulate susceptibility to PD in humans.
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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 Socratic graph.