By the abstracts:
"Are Expanded Polyglutamine Proteins a Proteasome Substrate?". Enquiry into whether the accumulation of polyglutamine aggregation that causes neurodegeneration is due to non-working proteasome function.
"Lifelong Aspirin Supplementation as a Means to Extending Life Span". Protocol proposal and rational for the experiment of what they suggest on the title. Not the results of such an experiment. Seems to focus mostly on the anti-inflammatory properties. Maybe interesting, although I would rather read the paper on the results of the experiment.
"Is Carnosine a Naturally Occurring Suppressor of Oxidative Damage in Olfactory Neurones?". What is says on the title.
A meeting report on "The 8th International Symposium on the Maillard Reaction (Charleston, South Carolina, August 28 to September 1, 2004)". Maillard reaction = glycation = non-enzimatic glycosylation. Didn't get to the meat, but I always like meeting reports.
A review of the book "Aging, Death, and Human Longevity: A Philosophical Inquiry" by Christine Overall (the book, not the review). Philosophy.
A review of the book "Aging, Death, and Human Longevity: A Philosophical Inquiry" by Gina Smith. Popular science.
Overall, I'm not as upset as usual at not having the papers for this one.
Monday, September 3, 2012
Sunday, September 2, 2012
Premature ageing in mice expressing defective mitochondrial DNA polymerase
Interestingness: 8
By Trifunovic A, Wredenberg A, Falkenberg M, Spelbrink JN, Rovio AT, Bruder CE, Bohlooly-Y M, Gidlöf S, Oldfors A, Wibom R, Törnell J, Jacobs HT and Larsson NG, in Nature, on the 27th of May, 2004. 429(6990):417-23. http://www.ncbi.nlm.nih.gov/pubmed/15164064
This isn't a paper from Rejuvenation Research, but since it was referenced in the last post, I read it and found it very interesting, notwithstanding de Grey's comments on it not being as interesting as it seems.
They created mice with a mutant version of the mtDNA polymerase instead of the regular version, that resulted in 3-5 times the usual number of mutations in their mtDNA and many more mtDNA deletions (30% less full-length mtDNA than wild type). Mutations were uniform throughout the whole mtDNA. The method of creating these mutant mice is interesting enough, but I won't describe that here.
These mice live for about a year. They have much smaller testes by the 3 month mark. They then get some fucked-up looking back deformations (kyphosis), start losing their hair, losing weight, become anaemic (with larger than usual and paler red blood cells), and get enlarged spleens by around the six-month mark. They develop osteoporosis and enlarged left ventricles at around the 9 month mark.
If de Grey's explanation is right then it's not significant, but if he is wrong, then mtDNA mutations become more important.
By Trifunovic A, Wredenberg A, Falkenberg M, Spelbrink JN, Rovio AT, Bruder CE, Bohlooly-Y M, Gidlöf S, Oldfors A, Wibom R, Törnell J, Jacobs HT and Larsson NG, in Nature, on the 27th of May, 2004. 429(6990):417-23. http://www.ncbi.nlm.nih.gov/pubmed/15164064
This isn't a paper from Rejuvenation Research, but since it was referenced in the last post, I read it and found it very interesting, notwithstanding de Grey's comments on it not being as interesting as it seems.
They created mice with a mutant version of the mtDNA polymerase instead of the regular version, that resulted in 3-5 times the usual number of mutations in their mtDNA and many more mtDNA deletions (30% less full-length mtDNA than wild type). Mutations were uniform throughout the whole mtDNA. The method of creating these mutant mice is interesting enough, but I won't describe that here.
These mice live for about a year. They have much smaller testes by the 3 month mark. They then get some fucked-up looking back deformations (kyphosis), start losing their hair, losing weight, become anaemic (with larger than usual and paler red blood cells), and get enlarged spleens by around the six-month mark. They develop osteoporosis and enlarged left ventricles at around the 9 month mark.
If de Grey's explanation is right then it's not significant, but if he is wrong, then mtDNA mutations become more important.
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