Thursday, May 4 | 12:00 – 12:20 | Auditorium
Thursday, May 4 | 14:00 – 15:00 | Auditorium
Cell aging, also known as cellular senescence, was first demonstrated to be caused by telomere shortening and dysfunction. It is now well stablished that short and damaged telomeres are associated, often in a causative manner, with several age-related severe human diseases and aging itself. Nevertheless, so far we lacked the means to blunt the consequences of telomere dysfunction. We will discuss an innovative approach, presently in preclinical development, effective in a variety of animal models of accelerated aging and age-related disorders.
Thursday, May 4 | 14:00 – 15:00 | Auditorium
The mechanistic Target of Rapamycin (mTOR) is an evolutionarily conserved regulator of longevity that plays a central role linking environmental cues to aging biology. The mTOR inhibitor rapamycin is currently the most effective and reproducible pharmacological approach to extending lifespan in animals. Several groups have independently shown that short-term treatment with rapamycin in mice can prevent age-related decline or rejuvenate functional measures of health in various organs and tissues including brain, heart, kidney, muscle, oral cavity, immune system, and ovary. Multiple clinical trials have been, or will soon be, initiated with the goal to determine whether rapamycin can positively impact age-related endpoints in humans and companion dogs. Several hundred “biohackers” are proactively using rapamycin off-label in hopes that it will increase healthspan and lifespan and a growing number of medical practitioners are prescribing rapamycin for such “off-label” use.
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