ArticleMolecular neurodegeneration2020
Circulating cell-free mitochondrial DNA levels in Parkinson's disease are influenced by treatment.
Article in Molecular neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
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Who cites it
57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.
- Mitochondrial DNA (mtDNA) as fluid biomarker in neurodegenerative disorders: A systematic review.European journal of neurology · 2025Pooled it
- Biomarkers of mitochondrial dysfunction in acute respiratory distress syndrome: A systematic review and meta-analysis.Frontiers in medicine · 2022Pooled 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
- Rethinking Mitochondrial Parkinson's Disease in the α-Synuclein Seed Amplification Assays Era.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Mitochondrial dysfunction in PTSD: A mechanism to understand trauma susceptibility?Psychopharmacology · 2026Review
- Mitochondrial DNA: a molecular switch driving sterile neuroinflammation.Translational neurodegeneration · 2026Review
- Mitophagy-NLRP3 Inflammasome Crosstalk in Parkinson's Disease: Pathogenic Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- The mitogenome mutation repertoire affects progression of Parkinson's Disease.Genetics and molecular biology · 2026Article
- CSF Mitochondrial DNA: Biomarker of Body Composition and Energy Metabolism in Parkinson's Disease.Annals of clinical and translational neurology · 2025Article
- Cell-Free DNA and Mitochondria in Parkinson's Disease.International journal of molecular sciences · 2025Review
- Integrated multi omics and machine learning reveal mitochondrial immunometabolic networks in sepsis associated encephalopathy.Scientific reports · 2025Article
- Micro- and nanoscale biosensing technologies for early diagnosis of Parkinson's disease.Mikrochimica acta · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025Review
- The Potential of cfDNA as Biomarker: Opportunities and Challenges for Neurodegenerative Diseases.Journal of molecular neuroscience : MN · 2025Review
- Diagnostic role of circulating cell-free DNA in schizophrenia and neuro-degenerative disorders.Biomarkers in medicine · 2025Review
- Liquid Biopsy in Neuropsychiatric Disorders: A Step Closer to Precision Medicine.Molecular neurobiology · 2025Review
- Parkinson's disease and glucose metabolism impairment.Translational neurodegeneration · 2025Review
- Cell-Free DNA, a Noninvasive Biomarker for Prediction and Detection of Neurodegenerative Diseases, New Insights, and Perspectives.CNS & neurological disorders drug targets · 2025Review
- Elevated serum circulating cell-free mitochondrial DNA in amyotrophic lateral sclerosis.European journal of neurology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Several studies have linked circulating cell-free mitochondrial DNA (ccf-mtDNA) to human disease. In particular, reduced ccf-mtDNA levels in the cerebrospinal fluid (CSF) of both Alzheimer's and Parkinson's disease (PD) patients have raised the hypothesis that ccf-mtDNA could be used as a biomarker for neurodegenerative disease onset and progression. However, how a reduction of CSF ccf-mtDNA levels relates to neurodegeneration remains unclear. Many factors are likely to influence ccf-mtDNA levels, such as concomitant therapeutic treatment and comorbidities. In this study we aimed to investigate these factors, quantifying CSF ccf-mtDNA from the Parkinson's Progression Markers Initiative in 372 PD patients and 159 matched controls at two time points. We found that ccf-mtDNA levels appear significantly reduced in PD cases when compared to matched controls and are associated with cognitive impairment. However, our data indicate that this reduction in ccf-mtDNA is also associated with the commencement, type and duration of treatment. Additionally, we found that ccf-mtDNA levels are associated with comorbidities such as depression and insomnia, however this was only significant if measured in the absence of treatment. We conclude that in PD, similar to reports in HIV and sepsis, comorbidities and treatment can both influence ccf-mtDNA homeostasis, raising the possibility that ccf-mtDNA may be useful as a biomarker for treatment response or the development of secondary phenotypes. Given that, clinically, PD manifests often decades after neurodegeneration begins, predicting who will develop disease is important. Also, identifying patients who will respond to existing treatments or develop secondary phenotypes will have increased clinical importance as PD incidence rises.
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Registered trials
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