Lowered dietary protein leads to a longer life, acting in much the same way as calorie restriction. Here researchers delve more deeply into the underlying mechanisms: “Mitochondria act as the ‘powerhouse’ of the cells. It is well known that mitochondrial function worsens with age in many species … Our study shows that dietary restriction can enhance mitochondrial function hence offsetting the age-related decline in its performance … The researchers report the unexpected finding that while there is a reduction in protein synthesis globally with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased … That activity, which takes place at the level of conversion of RNA to protein, is important for the protective effects of dietary restriction … There have been correlative studies that show mitochondria change with dietary restriction, this research provides a causal relationship between diet and mitochondrial function … mitochondrial genes are converted from RNA to protein by a particular protein (d4EBP). Flies fed a low protein diet showed an uptick in activity of d4EBP, which is involved in a signaling pathway that mediates cell growth in response to nutrient availability called TOR (target of rapamycin). … d4EBP is necessary for lifespan extension upon dietary restriction. When the activity of the protein was genetically ‘knocked out’ the flies did not live longer, even when fed the low protein diet. When the activity of d4EBP was enhanced, lifespan was extended, even when the flies ate a rich diet.”
View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-10/bifa-lp092409.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Continue Reading October 2nd, 2009
From Depressed Metabolism: “I think in the next 20 years more small animal organs, and perhaps some human organs, may be reversibly cryopreserved. The best scenario for cryonics would be improved, and possibly demonstrably reversible, cryopreservation of animal brains. It has been long observed that if reversible solid-state brain preservation could be demonstrated, then cryonics revival becomes a purely technical problem (albeit very complex one) of tissue regeneration. There would be no remaining doubt about whether the preservation itself was viably preserving human beings … Reversible solid-state cryopreservation of whole mammals is a very difficult problem with existing technology. This is why when asked about it people will often defer to nanotechnology. References to nanotechnology as a solution to a medical problem basically say, ‘We have no idea how to solve this problem with existing tools, but future abilities to completely analyze and repair tissue at the molecular level will be implicitly sufficient.’ It’s a valid argument, but saying that a medical problem will be solved when someday technology exists to solve every medical problem is not very illuminating about time lines or nature of the problem.”
View the Article Under Discussion: http://www.depressedmetabolism.com/2009/10/01/reversible-cryopreservation/
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Continue Reading October 2nd, 2009
I see that, thanks to the vigorous response of the pro-longevity community, the SENS Foundation has won $5,000 for longevity research: “The challenge, launched this September, was sponsored by 3banana as a philanthropic crowdsourcing contest helping health, environment and education-focused non-profit organizations raise money and exposure for their respective causes while testing the sharing features of the company’s online and mobile note-taking software. … ‘We are very honored to accept this prize. This contest has really opened our eyes to the possibilities of furthering our cause using social networks,’ said Dr. Aubrey de Grey, Chief Science Officer for the SENS Foundation. ‘Thousands of our supporters shared their words of encouragement for our mission, and this effort has created more dialog between our organization and our supporters.’” As the cost of biotech research falls, I think we’re going to see much more grassroots fundraising of this nature - see, for example, the laser ablation of lipofuscin research that was funded earlier this year via online efforts.
View the Article Under Discussion: http://www.prweb.com/releases/2009/09/prweb2968404.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Continue Reading October 1st, 2009
Via ScienceDaily: “adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell’s ability to divide. The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells’ capacity to effectively rebuild the body. This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. … For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly … When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced. … In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials.”
View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/09/090930084602.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Continue Reading October 1st, 2009
Here’s a long post on the utility of contributing to engineered longevity versus the other forseeable technology most likely to dramatically reshape the world - self-improving artificial intelligence (AI). The author puts that goal in advance of contributing now to advancing longevity science, but I think that a point is missed along the way. Even if your contributions made now don’t lead to technologies arriving in time to extend your life, they will bring forward the dates at which the medicine of engineered longevity does emerge in each region of the world. Every day gained in this fashion saves approximately 100,000 lives at present population levels. From the post: “The crux of my conflict is whether there is greater utility in putting money toward longevity or strong AI. … . And for now, let’s pretend that longevity escape velocity (LEV) occurs 25 years from now without any of my investment. Now lets say I buy 5 years of ‘progress’ in longevity, so it happens only 20 years from now. I think it’s likely that within the first few decades of LEV, most of the change in life expectancy will come from wealthy old people in prosperous nations. I just saved and improved many lives, but not a whole bunch … probably under half a billion. Infectious and lifestyle diseases, accidents and wars still exist, and those who can’t afford treatment still die when they get old, even when AI shows up.”
View the Article Under Discussion: http://raelifin.com/thoughts/on-the-utility-of-game-changing-technologies/
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Continue Reading September 30th, 2009
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