His decision came as an investigation into sexual harassment allegations against him was ongoing.
Increased collagen expression is a common feature of many different pathways to extended longevity in worms.
March 1, 2015|
COURTESY OF KEITH BLACKWELL
C.Y. Ewald et al., “Dauer-independent insulin/IGF-1-signalling implicates collagen remodelling in longevity,” Nature, doi:10.1038/nature14021, 2014.
One of the earliest observations about longevity in the roundworm Caenorhabditis elegans, a choice model organism for aging research, was that the worms live longer when the insulin/insulin-like growth factor 1 pathway is disrupted. This disruption normally sends worms into a hibernation-like state, called dauer, which increases life span by inserting a pause into the life cycle. Keith Blackwell of Boston’s Joslin Diabetes Center and colleagues wondered if blocking the insulin/IGF1 pathway could increase life span even without this hiatus.
To this end, the researchers reduced the insulin/IGF1 pathway at temperatures that block entry into the dauer state, and the worms still lived longer. The team looked for changes in gene expression that accompanied this phenomenon and found the most striking upregulation among collagen genes. Such an uptick in expression was not unique to disabling insulin signaling; Blackwell’s group found that collagens were also boosted in several other interventions that extended life span in C. elegans.
Collagens are most familiar as the proteins whose age-related dysfunction causes wrinkles. “This paper really suggests that collagens are not just, let’s say, associated with external, . . . cosmetic usefulness, but overall improved health,” says Malene Hansen of La Jolla’s Sanford-Burnham Medical Research Institute. The study also suggests a new role in aging for the extracellular matrix, where collagens are found. “Mechanisms that will extend life [may] act by enhancing the function of the extracellular matrices and specifically of collagens,” says Blackwell.
Whether collagen decline leads to aging or vice versa is an area for future research. “There’s likely to be sort of a feedback loop” between the two, says Hansen.
March 25, 2015
Aging results from accumulation of faulty damaged macromolecules mostly proteins. Rapamycin that increases both protein degradation and simultaneously protein synthesis leads to prolonged life, longevity. Michael Lerman, Ph.D., M.S.
March 25, 2015
Because deteriorating health as usually seen in aging people is the result of a plethora of knock-on (cumulatively cascading) effects owing to genetic, life-event (injury), self-infliction (sedentariness, drugs, tobacco and excessive alcohol), mental and other issues, there can be no "magic bullet" to reverse the process. It is likely that any purported 'cure' showing apparent improvement, such as rapamycin, will likely prove physiologically counterproductive (if not harmful) in the long haul.
However, everyone has built-in but neglected rejuvenators; to turn them "on," we have to create proper conditions to allow them to blossom. The process is simple, but imposes discomfort on those culturally conditioned to passively basting themselves in the effluent of modern entertainment via the spallation of electronic widgetry.
(We need more than a good Mediterranean diet, sociability and idea puzzling.) Because dynamism is the esential observable basis of life (there is no such thing as wasted action), we have to put ourselves in physical motion against various kinds of resistance in order to set our muscles and bones to working and flex our tissues to change the microenvironments of our cells causing them (the strong that survive) to rework their extracellular matrices and, voila, more collagen, healthier cells, improved functioning in the above categories and downtime, etc. Get hot. Now.
March 28, 2015