ArticleNeurobiology of aging2013
Frailty and mortality are not influenced by mitochondrial DNA haplotypes in the very old.
Article in Neurobiology of aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed.
- Perspectives on pharmacogenomics of antiretroviral medications and HIV-associated comorbidities.Current opinion in HIV and AIDS · 2015Review
- Mitochondrial genomes and exceptional longevity in a Chinese population: the Rugao longevity study.Age (Dordrecht, Netherlands) · 2015Article
- Article
- The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.Human genetics · 2014Review
- Article
- The three genetics (nuclear DNA, mitochondrial DNA, and gut microbiome) of longevity in humans considered as metaorganisms.BioMed research international · 2014Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Inherited genetic variation of mitochondrial DNA (mtDNA) could account for the missing heritability of human longevity and healthy aging. Here, we show no robust association between common genetic variants of mtDNA and frailty (an "unhealthy aging" phenotype) or mortality in 700, more than 85-year-old, participants of the Newcastle 85+ study. Conflicting data from different populations underscore our conclusion that there is currently no compelling link between inherited mtDNA variants and aging.
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Registered trials
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