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Mitochondrial DNA depletion in sporadic inclusion body myositis.

This group reports some interesting findings in patients with sporadic inclusion body myositis (sIBM), principal of which may be that "muscle from sIBM patients contained on average 67% less mtDNA than healthy controls (P = 0.001)." I wonder whether this might be related to the development of the disease.
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Increased dNTP pools rescue mtDNA depletion in human POLG-deficient fibroblasts.

Because this work was done in a model of POLG-deficiency, it's not clear to me that this has any relevance to age-related mtDNA problems. But the intervention and results were interesting and relevant to mtDNA maintenance, so I'm including it in case it is relevant. This group reported that increasing the concentration of deoxynucleotide triphosphates to mitochondria could restore mtDNA depletion in this model. They suggest this might be relevant for "other conditions in which mtDNA maintenance is challenged"; couldn't aging be characterized in this way? But perhaps aging is not characterized by POLG deficiency, so this particular intervention may not be useful.
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Mitochondrial – nuclear genetic interaction modulates whole body metabolism, adiposity and gene expression in vivo.

I thought perhaps the methods in this paper might be interesting to mitochondrial researchers. I didn't look into the full-text for details, but something the authors said in the abstract that may be of interest: "we used Mitochondrial-Nuclear eXchange mice, which have reciprocally exchanged nuclear and mitochondrial genomes between different Mus musculus strains." Moreover, this paper may have some interesting data about how the nuclear and mitochondrial genomes communicate with one another.
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Proliferation Cycle Causes Age Dependent Mitochondrial Deficiencies and Contributes to the Aging of Stem Cells.

I found this report particularly interesting because it's apparently related to two papers I recently reported on: (1) Muscle Stem Cells Exhibit Distinct Clonal Dynamics in Response to Tissue Repair and Homeostatic Aging (PMID 29249462) and mTORC1 activation during repeated regeneration impairs somatic stem cell maintenance (PMID 29220665). However, the current paper is about female reproduction in Drosophila. These researchers report that proliferation " causes an accumulation of mtDNA mutations or rearrangements at the control region ", therefore it may be that " damaging mutations on mtDNA caused by accumulation of proliferation cycles in aged stem cells may disrupt mitochondrial respiration chain and impair mtDNA replication and represent a conserved mechanism underlying stem cell aging ." Could the observation from PMID 29220665 that stem cell loss can be prevented with mTORC1 inhibition be relevant to reproductive aging?
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Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation.

I wonder if readers on this distribution list have already seen this association between mtDNA double-strand breaks and demyelination. If I recall correctly, I thought I've seen demyelination observed to be age-related. If so, could mtDNA damage be a primary cause? Or is this a case of there being many ways to induce a given dysfunction, and that this particular one is not likely to be occurring during human aging?
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