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Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging.

This group reports on some telomere and telomerase dynamics in the brains of aging mice. They observe that telomeres were shortened in old mice according to both proliferating and non-proliferating cell types. But this seems to be old news; I thought Oki told me years ago that during his PhD or post-doc work, he learned that the majority of telomere shortening was due to oxidative stress and other non-cell-cycle-related phenomena.
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Telomeres Increasingly Develop Aberrant Structures in Aging Humans.

This group reports that human telomeres display an increasing prevalence of aberrant structures during human aging. These aberrations include "sister telomere loss and sister telomere chromatid fusions" which "increased consistently throughout the entire human lifespan". If telomeres help regulate gene expression, these seem like concerning observations which may need to be addressed by rejuvenation interventions.
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Telomeres and Cell Senescence – Size Matters Not.

This looks like a potentially-interesting review of some mechanisms of cellular senescence related to telomeres. I found it especially interesting that these authors suggest in the abstract that "telomere-induced senescence may occur irrespectively of the length of telomeres".
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A balance between elongation and trimming regulates telomere stability in stem cells.

I retained this paper for my report primarily because of the mention of C-circles, suspecting that perhaps this discussion of telomere elongation and trimming might be an interesting read for ALT researchers. The mention of XRCC3 and Nbs1 might also be interesting, as the abstract notes the involvement of these proteins in "homologous recombination that generates single-stranded C-rich telomeric DNA..."
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The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence.

These authors report that the "telomeric protein" AKTIP is apparently involved in "lamin-related processes, including those that govern nuclear architecture, telomere homeostasis and cellular senescence". I report this here because I suspect that those groups working on addressing cellular senescence may find insight in this relationship between lamins, nuclear architecture, telomeres, and senescence, possibly giving clues about potential mechanisms of targeting or treating senescent cells.
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Analysis of alternative lengthening of telomere markers in BRCA1 defective cells.

These researchers report on their investigations of BRCA1, its association with PML bodies, and its possible relevance to alternative lengthening of telomeres (ALT). They found increased telomere recombination rates in cells from human BRCA1 mutation carriers, as well as mESC lacking functional copies of Brca1. They also report "elevated levels of ALT activity (via C-circle assay) in Brca1-defective mouse cells", and suggest that normal BRCA1 function may repress ALT, repression that is presumably disrupted with BRCA1 dysfunction. I also note, at least in the abstract, they did no t report elevated c-circles in cells from uman BRCA1 mutation carriers; I did not look at the full-text.
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