ArticleFrontiers in aging neuroscience2022
Mitochondrial DNA variation in Parkinson's disease: Analysis of "out-of-place" population variants as a risk factor.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- The mitogenome mutation repertoire affects progression of Parkinson's Disease.Genetics and molecular biology · 2026Article
- Mitochondrial DNA editing: Key to the treatment of neurodegenerative diseases.Genes & diseases · 2025Review
- Mitochondrial DNA Pathogenic Variant Prevalence in Primary Mitochondrial Disease Patients With African (L) Mitochondrial Genome Haplogroups.JIMD reports · 2025Article
- A nuclear-encoded endonuclease governs the paternal transmission of mitochondria in Cucumis plants.Nature communications · 2025Article
- Fish Models for Exploring Mitochondrial Dysfunction Affecting Neurodegenerative Disorders.International journal of molecular sciences · 2023Review
- Mitochondrial DNAFrontiers in ophthalmology · 2023Article
- Combination of common mtDNA variants results in mitochondrial dysfunction and a connective tissue dysregulation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
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Abstract
Mitochondrial DNA (mtDNA), a potential source of mitochondrial dysfunction, has been implicated in Parkinson's disease (PD). However, many previous studies investigating associations between mtDNA population variation and PD reported inconsistent or contradictory findings. Here, we investigated an alternative hypothesis to determine whether mtDNA variation could play a significant role in PD risk. Emerging evidence suggests that haplogroup-defining mtDNA variants may have pathogenic potential if they occur "out-of-place" on a different maternal lineage. We hypothesized that the mtDNA of PD cases would be enriched for out-of-place variation in genes encoding components of the oxidative phosphorylation complexes. We tested this hypothesis with a unique dataset comprising whole mitochondrial genomes of 70 African ancestry PD cases, two African ancestry control groups (
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Registered trials
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