Laura C. Greaves

TL;DR: This review considers the basic principles of mitochondrial genetics which govern both the behaviour and investigation of pathogenic mtDNA mutations summarizing recent advances, and an assessment of the ongoing debate into the role of somatic mt DNA mutations in neurodegenerative disease, ageing and cancer.

TL;DR: It is shown that chronic, progressive low-grade inflammation induced by knockout of the nfkb1 subunit of the transcription factor NF-κB induces premature ageing in mice, and frequency of senescent cells in liver and intestinal crypts quantitatively predict mean and maximum lifespan in both short- and long-lived mice cohorts.

TL;DR: The accumulation of mtDNA mutations in human colonic crypt stem cells that result in a significant biochemical defect in their progeny are described, which has important consequences not only for understanding of the finding of mt DNA mutations in aging tissues and tumors, but also for determining the frequency ofmtDNA mutations within a cell.

TL;DR: The results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.

TL;DR: It is demonstrated definitively that crypt fission is the mechanism by which mutations spread in the normal human colon, which has important implications for the biology of the normal adult human colon and possibly for the growth and spread of colorectal neoplasms.