ArticleScientific reports2022
Mitochondrial biogenesis, telomere length and cellular senescence in Parkinson's disease and Lewy body dementia.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- Association between mitochondrial DNA copy number and the risk of Parkinson's disease: a meta-analysis and Mendelian randomization study.BMC neurology · 2025Pooled it
- Mitochondrial DNA (mtDNA) as fluid biomarker in neurodegenerative disorders: A systematic review.European journal of neurology · 2025Pooled it
- Preliminary insights into whole-blood mitochondrial DNA copy number and telomere length in Parkinson's disease and multiple system atrophy.Journal of neurology · 2026Article
- Reduced Mitochondrial DNA Copy Number and Telomere Length in Essential Tremor Patients: Evidence from an Age- and Sex-Adjusted Cross-Sectional Case-Control Study.International journal of molecular sciences · 2026Article
- Association between leukocyte telomere length and neurodegenerative diseases: a prospective cohort in the UK Biobank.Journal of neurology · 2026Article
- Adjunctive EGb 761 treatment in patients with Parkinson's disease: a case series.Frontiers in aging neuroscience · 2026Article
- Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders.Frontiers in aging · 2026Review
- Genetic factors and comorbid pathologies interact to drive regional mitophagy alterations in Lewy body dementia.Acta neuropathologica · 2025Article
- Gestational phthalate levels and biomarkers of aging in infants and children from New York City.Environmental research · 2025Article
- Investigating the ageing-Parkinson's disease nexus: standardisation of in vitro models and techniques by the PD-AGE network.NPJ Parkinson's disease · 2025Review
- Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein.Molecular neurodegeneration · 2025Review
- The silent saboteur: oxidative stress and the path to cognitive dysfunction.Neurodegenerative disease management · 2025Review
- A Transcriptomic Roadmap of Parkinson's Disease Progression at Single Cell Resolution.medRxiv : the preprint server for health sciences · 2025Article
- Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?Nature reviews. Neurology · 2025Review
- Role of Cellular Senescence in Parkinson's Disease: Potential for Disease-Modification Through Senotherapy.Biomedicines · 2025Review
- Aging, cellular senescence and Parkinson's disease.Journal of Parkinson's disease · 2025Review
- Premature aging and metabolic diseases: the impact of telomere attrition.Frontiers in aging · 2025Review
- Cerebellum mitochondrial DNA copy number is increased in Parkinson's disease.Brain communications · 2025Article
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
- The Role of Mitochondrial Copy Number in Neurodegenerative Diseases: Present Insights and Future Directions.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive age is the single major risk factor for neurodegenerative diseases. Cellular aging markers during Parkinson's disease (PD) have been implicated in previous studies, however the majority of studies have investigated the association of individual cellular aging hallmarks with PD but not jointly. Here, we have studied the association of PD with three aging hallmarks (telomere attrition, mitochondrial dysfunction, and cellular senescence) in blood and the brain tissue. Our results show that PD patients had 20% lower mitochondrial DNA copies but 26% longer telomeres in blood compared to controls. Moreover, telomere length in blood was positively correlated with medication (Levodopa Equivalent Daily Dose, LEDD) and disease duration. Similar results were found in brain tissue, where patients with Parkinson's disease (PD), Parkinson's disease dementia (PDD) and Dementia with Lewy Bodies (DLB) showed (46-95%) depleted mtDNA copies, but (7-9%) longer telomeres compared to controls. In addition, patients had lower mitochondrial biogenesis (PGC-1α and PGC-1β) and higher load of a cellular senescence marker in postmortem prefrontal cortex tissue, with DLB showing the highest effect among the patient groups. Our results suggest that mitochondrial dysfunction (copy number and biogenesis) in blood might be a valuable marker to assess the risk of PD. However, further studies with larger sample size are needed to evaluate these findings.
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