Mitochondrial DNA (mtDNA) is maternally inherited. After birth, secondary mtDNA defects can arise. MtDNA depletion is a reduction in the amount of mtDNA in particular tissues. Multiple deletions of mtDNA accumulate as somatic mutations in mainly postmitotic tissues. These disorders of mtDNA maintenance frequently show Mendelian inheritance. Positional cloning has identified several genes involv...

The pathogenesis of sepsis is complex. Mitochondrial dysfunction, which is responsible for energy metabolism, intrinsic apoptotic pathway, oxidative stress, and systemic inflammatory responses, is closely related with severe sepsis induced death. Mitochondria DNA (mtDNA) contain un-methylated cytosine phosphate guanine (CpG) motifs, which exhibit immune stimulatory capacities. The aim of this s...

Mitochondrial DNA (mtDNA) mutations can result in mitochondrial dysfunction, but emerging experimental data question the fundamental role of mtDNA mutagenesis in age-associated mitochondrial impairment. The multicopy nature of mtDNA renders the impact of a given mtDNA mutation unpredictable. In this study, we compared mtDNA stability and mtRNA integrity during normal aging. Seven distinct sites...

BACKGROUND Traumatic brain injury (TBI) has been shown to activate the peripheral innate immune system and systemic inflammatory response, possibly through the central release of damage associated molecular patterns (DAMPs). Our main purpose was to gain an initial understanding of the peripheral mitochondrial response following TBI, and how this response could be utilized to determine cerebral ...

Since Szilard's seminal 1959 article, the role of accumulating nuclear DNA (nDNA) damage -- whether as mutations, i.e. changes to sequence, or as epimutations, i.e. adventitious but persistent alterations to methylation and other decorations of nDNA and histones -- has been widely touted as likely to contribute substantially to the aging process throughout the animal kingdom. Such damage certai...

The study of Mercer et al,1 published in this issue of Circulation Research, reports new evidence linking oxidative DNA damage, atherosclerosis, and the metabolic syndrome. Although these relationships have been long proposed,2–4 many have criticized previous reports asking the rhetorical question: Which came first, the chicken or the egg? Another question, more specific to the topic of the stu...

The study of Mercer et al,1 published in this issue of Circulation Research, reports new evidence linking oxidative DNA damage, atherosclerosis, and the metabolic syndrome. Although these relationships have been long proposed,2–4 many have criticized previous reports asking the rhetorical question: Which came first, the chicken or the egg? Another question, more specific to the topic of the stu...

Defects in mitochondrial oxidative phosphorylation have frequently been associated with Alzheimer's disease (AD), and both inherited and somatic mtDNA mutations have been reported in certain AD cases. To determine whether mtDNA mutations contribute more generally to the etiology of AD, we have investigated the sequence of the mtDNA control region (CR) from AD brains for possible disease-causing...

Variants in mitochondrial DNA (mtDNA) and nuclear genes encoding mitochondrial proteins in bipolar disorder, depression, or other psychiatric disorders have been studied for decades, since mitochondrial dysfunction was first suggested in the brains of patients with these diseases. Candidate gene association studies initially resulted in findings compatible with the mitochondrial dysfunction hyp...