ArticleHuman genetics2006
Does the mitochondrial genome play a role in the etiology of Alzheimer's disease?
Article in Human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis 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
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.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- No consistent evidence for association between mtDNA variants and Alzheimer disease.Neurology · 2012Pooled it
- Retrospective analysis of phytoSERM for management of menopause-associated vasomotor symptoms and cognitive decline: a pilot study on pharmacogenomic effects of mitochondrial haplogroup and APOE genotype on therapeutic efficacy.Menopause (New York, N.Y.) · 2020Trial
- Metabolomic Analysis of Aqueous Humor to Predict Glaucoma Progression and Overall Survival After Glaucoma Surgery-The MISO II Study.Metabolites · 2026Article
- Hormonal modulation, mitochondria and Alzheimer's prevention: the role of GLP-1 agonists and estrogens.Frontiers in molecular biosciences · 2025Review
- Mitochondrial DNA and Alzheimer's disease: a first case-control study of the Tunisian population.Molecular biology reports · 2022Article
- Article
- The heterogeneity among subgroups of haplogroup J influencing Alzheimer's disease risk.Journal of advanced research · 2021Article
- Mitochondrial genome variation in male LHON patients with the m.11778G > A mutation.Metabolic brain disease · 2020Article
- Exploratory analysis of mtDNA haplogroups in two Alzheimer's longitudinal cohorts.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- The Role of Mitochondria in Neurodegenerative Diseases: the Lesson from Alzheimer's Disease and Parkinson's Disease.Molecular neurobiology · 2020Review
- MtDNA population variation in Myalgic encephalomyelitis/Chronic fatigue syndrome in two populations: a study of mildly deleterious variants.Scientific reports · 2019Article
- New mtDNA Association Model, MutPred Variant Load, Suggests Individuals With Multiple Mildly Deleterious mtDNA Variants Are More Likely to Suffer From Atherosclerosis.Frontiers in genetics · 2018Article
- Clinically proven mtDNA mutations are not common in those with chronic fatigue syndrome.BMC medical genetics · 2017Article
- Biocomplexity and Fractality in the Search of Biomarkers of Aging and Pathology: Focus on Mitochondrial DNA and Alzheimer's Disease.Aging and disease · 2017Article
- Triad of Risk for Late Onset Alzheimer's: Mitochondrial Haplotype, APOE Genotype and Chromosomal Sex.Frontiers in aging neuroscience · 2016Review
- Alzheimer's pathogenesis and its link to the mitochondrion.Oxidative medicine and cellular longevity · 2015Review
- Mitochondrial genome changes and neurodegenerative diseases.Biochimica et biophysica acta · 2014Review
- Energy failure: does it contribute to neurodegeneration?Annals of neurology · 2013Review
- Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease.Free radical biology & medicine · 2013Article
- Tissue-specific implications of mitochondrial alterations in aging.Frontiers in bioscience (Elite edition) · 2013Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
We report here the analyses of complete mtDNA coding region sequences from more than 270 Alzheimer's disease (AD) patients and normal controls to determine if inherited mtDNA mutations contribute to the etiology of AD. The AD patients and normal individuals were carefully screened and drawn from two populations of European descent in an effort to avoid spurious effects due to local population anomalies. Overall, there were no significant haplogroup associations in the combined AD and normal control sequence sets. Reduced median network analysis revealed that the AD mtDNA sequences contained a higher number of substitutions in tRNA genes, and that there was an elevated frequency of replacement substitutions in the complex I genes of the control sequences. Analysis of the replacement substitutions indicated that those arising in the AD mtDNAs were no more deleterious, on average, than those in the control mtDNAs. The only evidence for the synergistic action of mutations was the presence of both a rare non-conservative replacement substitution and a tRNA mutation in 2 AD mtDNAs, from a total of 145, whereas such a combination of mutations was not observed in the control sequences. Overall, the results reported here indicate that pathogenic inherited mtDNA mutations do not constitute a major etiological factor in sporadic AD. At most, a small proportion of AD patients carry a pathogenic mtDNA mutation and a small proportion of cognitively normal aged individuals carry a mtDNA mutation that reduces the risk of AD.
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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.