ArticleNature aging2025
A blood-based DNA damage signature in patients with Parkinson's disease is associated with disease progression.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 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.
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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
6 citing papers in PubMed.
- Oligodendroglial somatic SNCA copy number gains are associated with inclusions and disease onset in multiple system atrophy.Acta neuropathologica · 2026Article
- Mitochondrial toxins cause widespread downregulation of pathways in X-linked dystonia-parkinsonism patient-derived neurons.Stem cell reports · 2026Article
- Impacts of DNA ligase I genotypes on Taiwan Parkinson's disease.BioMedicine · 2026Article
- Longitudinal assessment of DNA repair signature trajectory in prodromal versus established Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Folic acid prevents inner hair cell degeneration via genomic stability.Cell death discovery · 2025Article
- Sex-Specific Association Between XPC rs2228001 Polymorphism and Parkinson's Disease Risk in a Mexican Population: A Case-Control Study Exploring Gene-Environment Interactions.Brain sciences · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Aging is the main risk factor for Parkinson's disease (PD), yet our understanding of how age-related mechanisms contribute to PD pathophysiology remains limited. We conducted a longitudinal analysis of blood samples from the Parkinson's Progression Markers Initiative cohort to investigate DNA damage in PD. Patients with PD exhibited disrupted DNA repair pathways and biased suppression of longer transcripts, indicating age-related, transcription-stalling DNA damage. Notably, at the intake visit, this DNA damage signature was detected only in patients with more severe progression of motor symptoms over 3 years, suggesting its potential as a predictor of disease severity. We validated this signature in independent PD cohorts and confirmed increased DNA damage in peripheral blood cells and dopamine neurons of the substantia nigra pars compacta in postmortem PD brains. Our study sheds light on an aging-related mechanism in PD pathogenesis and identifies potential markers of disease progression, providing a diagnostic platform to prognosticate disease progression.
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