Aging gene - TOR
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MZ-5-156 [is] a “growth hormone-releasing hormone (GHRH) antagonist.” [Scientists] conducted their research in the SAMP8 mouse model, a strain engineered for studies of the aging process. They found that MZ-5-156 had positive effects on oxidative stress in the brain, improving cognition, telomerase activity (the actions of an enzyme which protects DNA material) and life span, while decreasing tumor activity.
Genetic Fountain of Youth - Technology Review
Article on Tor pathway in mice.
less than 3 percent of the budget of the National Institute on Aging, the key source of major funding in this country for research on aging, is spent on studying the fundamental biology of aging—and that’s a liberal estimate. Over 50 percent of its budget is devoted to Alzheimer’s-disease research. I am not arguing that we stop research on Alzheimer’s. I’m simply pointing out the fact that there is an enormous difference between research on aging and age-related diseases. If you cured Alzheimer’s tomorrow, it would add about three weeks on to the average life expectancy in this country.
Leonard Hayflick via Can Aging Be Solved? - Technology Review
Yeah, it’s a little ridiculous that we spend so little money on the biology of aging.
Cocktail of amino acids does wonders for mice | Seattle Times Newspaper
Want to live longer? … mice began drinking the BCAA water instead of regular water when they were 9 months old and kept drinking it for the rest of their lives. Those lives turned out to be significantly longer than for mice that drank normal water: a median of 869 days versus 774 days. The extra time amounted to a 12 percent increase in life span. The amino acids apparently boosted the mitochondria — often dubbed the power plants of cells — in the rodents’ skeletal and cardiac muscles. Their treadmill endurance improved, as did their motor coordination.
David Stipp: Why Anti-Aging Science Really Matters
Last year, for instance, research convincingly showed for the first time that a drug could extend life span in mammals. That has momentous implications, but I bet you can’t name the drug. Give up? It’s rapamycin, a medicine prescribed to prevent rejection of transplanted organs. Despite its reputation as an immune inhibitor, earlier studies with worms and flies suggested that it might mimic the anti-aging effects of calorie restriction, a curtailing of food intake that has long been known to brake aging in rodents and many other species. And when researchers at three different U.S. labs gave it to late-middle-aged mice, the results were stunning: the life expectancy of the aged males was boosted by 28 percent, and that of females by 38 percent.
consider this: if we were able to totally eliminate cancer, U.S. life expectancy would rise by only about three years. (The reason the gain would be so small is that the risk of many fatal diseases soars after age 65, so even if we were suddenly immune to cancer, those other killers would prevent average life span from rising much.)
Immortal Stem Cells for Anti-Aging Therapies - Life Extension
“four transcription factors that are active in embryonic stem cells and inactive in virtually all body cell types—Oct4, Sox2, Lin28, and Nanog.”
put these in a normal cell and turn it into a stem cell. Next step (which hasn’t totally been figured out) is how to use telomerase to lengthen the telomeres.
Eat less to live longer? Or eat less protein to live longer? - health - 03 June 2010 - New Scientist
[If fruit flies and rats ] are fed special diets with less amino acids - the building blocks of proteins - they can eat as many calories as they want and still live longer. “These results clearly show that you don’t need to restrict calories as a whole to get lifespan extension,” says Piper, an author of the study on flies (Nature, vol 462, p 1061). Further support for this idea comes from studying the molecular pathways inside cells that affect lifespan. A molecule called TOR has been found to set off a chain of reactions that boost cell growth at the expense of longevity. Blocking TOR increases lifespan in all organisms studied to date, including yeast and mice (Aging Cell, vol 9, p 105). Crucially, the most potent activators of TOR are amino acids. ”[CRONies are people who cut back on the amount of food they eat in hopes of living longer]
Where does the protein theory leave the CRONies? Fontana noticed that the people in his study group were eating high levels of protein, about 1.7 grams per kilogram of body weight per day. This is more than the US government-recommended intake of 0.8 g/kg/day, and higher than that in a typical American’s diet, about 1.2 g/kg/day.
So Fontana asked six CRONies to cut their protein intake to 0.95 g/kg/day while maintaining their usual calorie intake. After only three weeks on the low-protein diet, the CRONies showed a 25 per cent drop in their levels of IGF-1 (Aging Cell, vol 7, p 681). “Even if the CRONies are restricting their calories severely, if they’re eating a high-protein diet, they’re probably negating some of the most important beneficial effects,” says Fontana.
If the new theory is right, then the whole concept of calorie restriction needs to be rethought. The very term would be misleading; Fontana and others have started referring to dietary restriction instead. As news of the study has spread, some CRONies have already reduced their protein intake.
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Metformin also blocks TOR, and lengthens lifespan in worms and mice (Cell Metabolism, vol 11, p 390). Does metformin slow ageing in people too? Studies published earlier this year suggest that diabetics taking metformin do get less cancer (Diabetes Care, vol 33, p 322). “The major risk factor for cancer, above all others, is ageing,” says David Gems at University College London. He calls the studies a “smoking gun of a more generalised effect of metformin on ageing, rather than just strictly diabetes”.
via kurzweil
Learning from Werner Syndrome
“a gene shown to play a role in the aging process appears to play a role in the regulation of the differentiation of embryonic stem cells. … researchers identified a protein interaction that controls the silencing of Oct4, a key transcription factor that is critical to ensuring that embryonic stem cells remain pluripotent. The protein, WRNp, is the product of a gene associated with Werner syndrome, an autosomal recessive disorder hallmarked by premature aging. … We showed that the depletion of WRNp blocked the recruitment of Dnmt3b to the Oct4 promoter, and resulted in reduced methylation. The reduced DNA methylation was associated with continued Oct4 expression, which resulted in attenuated differentiation. … These results reveal a novel function of WRNp, and demonstrate that WRNp controls a key step in pluripotent stem cell differentiation. Our data support the emerging hypothesis that attenuated stem cell differentiation is involved in aging. This lack of differentiated cells may contribute to failure to maintain organ or tissue function in the later stages of life.”
To me….very interesting…not enough people and money are focused on aging research.
quote comes from this article originally
Stereotypes about aging may be bad for your health — or good for it - The Boston Globe
who expressed gloomy views about elders when they were younger were much more likely to suffer a heart attack, stroke, or other cardiac problem 30 years later, compared to those who held more benign opinions. Specifically, 25 percent of those in the negative age-stereotype group had experienced a heart problem, compared to just 13 percent in the positive age-stereotype group, even taking into account variables such as blood pressure, smoking, and cholesterol levels.
The findings build on Levy’s earlier work, which revealed that negative images of aging can increase stress, while positive ones can be calming.
Levy, the Yale researcher, has found that people older than 50 with more positive self-perceptions of aging, measured up to 23 years earlier, lived 7.5 years longer than those with less positive views.
power of thinking….
BBC NEWS | Health | Running 'can slow ageing process'
The work tracked 500 older runners for more than 20 years, comparing them to a similar group of non-runners. All were in their 50s at the start of the study. Nineteen years into the study, 34% of the non-runners had died compared to only 15% of the runners. Both groups became more disabled with age, but for the runners the onset of disability started later - an average of 16 years later. The health gap between the runners and non-runners continued to widen even as the subjects entered their ninth decade of life. If you had to pick one thing to make people healthier as they age, it would be aerobic exercise Lead author Professor James Fries Running not only appeared to slow the rate of heart and artery related deaths, but was also associated with fewer early deaths from cancer, neurological disease, infections and other causes. And there was no evidence that runners were more likely to suffer osteoarthritis or need total knee replacements than non-runners - something scientists have feared. At the beginning of the study, the runners ran for about four hours a week on average. After 21 years, their weekly running time had reduced to around 76 minutes, but they were still seeing health benefits from taking regular exercise.
Kind of a cool study, but we don’t know if those who run also eat better etc., but it’s still kind of cool that this study quantifies that these runners have 16 more years of healthy life before disability sets in - 16 years is staggering….
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