ArticleMetabolic brain disease2017
Mitochondrial DNA levels in Huntington disease leukocytes and dermal fibroblasts.
Article in Metabolic brain disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Mitochondrial DNA homeostasis: A novel therapeutic target for neurodegenerative diseases.Neural regeneration research · 2026Article
- Mitochondrial morphology and mtDNA content in fibroblasts from patients with different types of mucopolysaccharidosis.Acta biochimica Polonica · 2026Article
- Diagnostic role of circulating cell-free DNA in schizophrenia and neuro-degenerative disorders.Biomarkers in medicine · 2025Review
- Sex contribution to average age at onset of Huntington's disease depends on the number of (CAG)Scientific reports · 2024Article
- Review
- Huntington's disease affects mitochondrial network dynamics predisposing to pathogenic mitochondrial DNA mutations.Brain : a journal of neurology · 2024Article
- The Role of Mitochondrial Copy Number in Neurodegenerative Diseases: Present Insights and Future Directions.International journal of molecular sciences · 2024Review
- Correction of symptoms of Huntington disease by genistein through FOXO3-mediated autophagy stimulation.Autophagy · 2024Article
- mtDNA Maintenance and Alterations in the Pathogenesis of Neurodegenerative Diseases.Current neuropharmacology · 2023Review
- Insights into Manganese Superoxide Dismutase and Human Diseases.International journal of molecular sciences · 2022Review
- The use of fibroblasts as a valuable strategy for studying mitochondrial impairment in neurological disorders.Translational neurodegeneration · 2022Review
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Mitochondrial Epigenetics and Environmental Health: Making a Case for Endocrine Disrupting Chemicals.Toxicological sciences : an official journal of the Society of Toxicology · 2020Review
- Thinking outside the nucleus: Mitochondrial DNA copy number in health and disease.Mitochondrion · 2020Review
- Genistein induces degradation of mutant huntingtin in fibroblasts from Huntington's disease patients.Metabolic brain disease · 2019Article
- Mitochondrial alterations accompanied by oxidative stress conditions in skin fibroblasts of Huntington's disease patients.Metabolic brain disease · 2018Article
- Increased nuclear DNA damage precedes mitochondrial dysfunction in peripheral blood mononuclear cells from Huntington's disease patients.Scientific reports · 2018Article
- Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018Review
- The role of STING signaling in central nervous system infection and neuroinflammatory disease.WIREs mechanisms of diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington disease (HD) is an inherited neurodegenerative disorder caused by mutations in the huntingtin gene. Involvement of mitochondrial dysfunctions in, and especially influence of the level of mitochondrial DNA (mtDNA) on, development of this disease is unclear. Here, samples of blood from 84 HD patients and 79 controls, and dermal fibroblasts from 10 HD patients and 9 controls were analysed for mtDNA levels. Although the type of mitochondrial haplogroup had no influence on the mtDNA level, and there was no correlation between mtDNA level in leukocytes in HD patients and various parameters of HD severity, some considerable differences between HD patients and controls were identified. The average mtDNA/nDNA relative copy number was significantly higher in leukocytes, but lower in fibroblasts, of symptomatic HD patients relative to the control group. Moreover, HD women displayed higher mtDNA levels in leukocytes than HD men. Because this is the largest population analysed to date, these results might contribute to explanation of discrepancies between previously published studies concerning levels of mtDNA in cells of HD patients. We suggest that the size of the investigated population and type of cells from which DNA is isolated could significantly affect results of mtDNA copy number estimation in HD. Hence, these parameters should be taken into consideration in studies on mtDNA in HD, and perhaps also in other diseases where mitochondrial dysfunction occurs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.