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Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers.
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High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease.
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Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons.
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Double-strand breaks of mouse muscle mtDNA promote large deletions similar to multiple mtDNA deletions in humans.
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Two direct repeats cause most human mtDNA deletions.
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Twinkle and POLG defects enhance age-dependent accumulation of mutations in the control region of mtDNA.
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Mitochondrial enzyme-deficient hippocampal neurons and choroidal cells in AD.
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Coupled leading- and lagging-strand synthesis of mammalian mitochondrial DNA.
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Cytochrome c oxidase defects of the human substantia nigra in normal aging.
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