Lisbon, Portugal • May 4-5, 2023


Thursday, May 4  | 12:00 – 12:20 | Auditorium

The Role of Telomeres in Aging

by Maria A. Blasco, PhD, Scientific Director of the Spanish National Cancer Research Centre (CNIO), Madrid, Spain

Thursday, May 4  | 14:00 – 15:00 | Auditorium

Quantification of Biological Aging

by Daniel W. Belsky, Assistant Professor of Epidemiology, The Robert N. Buttler Columbia Aging Center , Columbia University, New York, USA

Biological aging is the progressive loss of system integrity that occurs with advancing age, undermining the integrity and resilience of tissues and organ systems and driving vulnerability to disease, disability, and death. Animal experiments suggest that biological aging is is caused by an accumulation of cellular-level molecular changes, sometimes referred to as hallmarks, that, when slowed or reversed, result in increased healthy lifespan. Human translation of therapies to modify hallmarks of aging and extend healthy lifespan is a critical priority for an aging global population. To speed this translation, measurements that quantify the progress and pace of biological aging in humans are needed. The past several years have seen rapid progress toward this goal, with measurements based on micro-array assays of DNA methylation marks representing the current state of the art. My talk will review progress and challenges in this effort, share some of our work to develop a DNA methylation biomarker of the pace of biological aging, DunedinPACE, and report results from biological aging analysis of the CALERIE Trial, a randomized controlled trial of caloric restriction in healthy, non-obese midlife humans. 

Thursday, May 4  | 14:00 – 15:00 | Auditorium

Telomeres and Biology of Aging

by Fabrizio d’Adda di Fagagna, PhD, Principal Investigator of Institute of Molecular Genetics (CNR), Pavia, Italy

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

Toward Clinical Evaluation of mTOR inhibitors to Target Biological Aging

by Matt Kaeberlein, PhD, Professor of Genome Sciences, University of Washington, Seattle, WA, USA

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.