ArticleCellular and molecular neurobiology2007
Huntington's disease and mitochondrial DNA deletions: event or regular mechanism for mutant huntingtin protein and CAG repeats expansion?!
Article in Cellular and molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Huntington's disease in MENAT: systematic review and meta-analysis of prevalence, clinical features, and genetics.Journal of neurology · 2025Pooled it
- Advances in research on mitochondrial dysfunction in neurodegenerative diseases.Journal of neurology · 2025Review
- Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation.Frontiers in immunology · 2025Review
- Review
- Mitochondrial Abnormalities and Synaptic Damage in Huntington's Disease: a Focus on Defective Mitophagy and Mitochondria-Targeted Therapeutics.Molecular neurobiology · 2021Review
- Age-related mitochondrial alterations in brain and skeletal muscle of the YAC128 model of Huntington disease.NPJ aging and mechanisms of disease · 2021Article
- Understanding the Multiple Role of Mitochondria in Parkinson's Disease and Related Disorders: Lesson From Genetics and Protein-Interaction Network.Frontiers in cell and developmental biology · 2021Review
- Mitochondrial Dysfunctions: A Red Thread across Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Deterioration of mitochondrial bioenergetics and ultrastructure impairment in skeletal muscle of a transgenic minipig model in the early stages of Huntington's disease.Disease models & mechanisms · 2019Article
- Review
- Analyses of Mitochondrial DNA and Immune Phenotyping Suggest Accelerated T-Cell Turnover in Treated HIV.Journal of acquired immune deficiency syndromes (1999) · 2018Article
- Recent Progress in Vascular Aging: Mechanisms and Its Role in Age-related Diseases.Aging and disease · 2017Review
- Increased mitochondrial fission and neuronal dysfunction in Huntington's disease: implications for molecular inhibitors of excessive mitochondrial fission.Drug discovery today · 2014Review
- Mitochondria as a therapeutic target for aging and neurodegenerative diseases.Current Alzheimer research · 2011Review
- Huntington's disease and mitochondrial alterations: emphasis on experimental models.Journal of bioenergetics and biomembranes · 2010Article
- Abnormal mitochondrial dynamics--a novel therapeutic target for Alzheimer's disease?Molecular neurobiology · 2010Review
- Basic mechanisms of neurodegeneration: a critical update.Journal of cellular and molecular medicine · 2010Review
- 3-Nitropropionic acid as a tool to study the mechanisms involved in Huntington's disease: past, present and future.Molecules (Basel, Switzerland) · 2010Review
- Abnormal mitochondrial dynamics and neurodegenerative diseases.Biochimica et biophysica acta · 2010Review
- Recent advances in our understanding of neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial DNA (mtDNA) may play an essential role in the pathogenesis of the respiratory chain complex activities in neurodegenerative disorders such as Huntington's disease (HD). Research studies were conducted to determine the possible levels of mitochondrial defect (deletion) in HD patients and consideration of interaction between the expanded Huntingtin gene as a nuclear gene and mitochondria as a cytoplasmic organelle. To determine mtDNA damage, we investigated deletions based in four areas of mitochondrial DNA, in a group of 60 Iranian patients clinically diagnosed with HD and 70 healthy controls. A total of 41 patients out of 60 had CAG expansion (group A). About 19 patients did not show expansion but had the clinical symptoms of HD (group B). MtDNA deletions were classified into four groups according to size; 9 kb, 7.5 kb, 7 kb, and 5 kb. We found one of the four-mtDNA deletions in at least 90% of samples. Multiple deletions have also been observed in 63% of HD patients. None of the normal control (group C) showed mtDNA deletions. The sizes or locations of the deletions did not show a clear correlation with expanded CAG repeat and age in our samples. The study presented evidence that HD patients had higher frequencies of mtDNA deletions in lymphocytes in comparison to the controls. It is thus proposed that CAG repeats instability and mutant Htt are causative factor in mtDNA damage.
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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.