ARDD 2026 has announced that Fiona Marshall, President of Biomedical Research at Novartis, will deliver a featured presentation, "Reimagining Drug Discovery Through the Lens of Aging Biology," at the 13th Aging Research & Drug Discovery (ARDD) Meeting, taking place October 1–3, 2026, at Harvard University's David Rubenstein Treehouse in Boston. As the world's leading conference dedicated to longevity biotechnology, ARDD 2026 will convene top researchers, pharmaceutical executives, entrepreneurs, and investors to accelerate the translation of aging science into next-generation medicines.

ARDD 2026 has announced that Fiona Marshall, President of Biomedical Research at Novartis, will deliver a featured presentation, "Reimagining Drug Discovery Through the Lens of Aging Biology," at the 13th Aging Research & Drug Discovery (ARDD) Meeting, taking place October 1–3, 2026, at the David Rubenstein Treehouse at Harvard University. As the world's leading conference dedicated to longevity biotechnology, ARDD 2026 will convene top researchers, pharmaceutical executives, entrepreneurs, and investors to accelerate the translation of aging science into next-generation medicines.

Organized by Insilico Medicine and supported by industry leaders including Eli Lilly and the McKinsey Health Institute, the meeting reflects the growing momentum behind longevity as a major frontier in biomedical innovation. With speakers representing ten of the world's leading pharmaceutical companies, ARDD 2026 aims to foster the collaborations needed to transform discoveries in aging biology into therapies that extend healthy lifespan and improve patient outcomes.

With the support of National Institutes of Health funding, Johns Hopkins Medicine investigators, led by pathologist Aaron W. James, M.D., Ph.D., previously discovered that sensory neurons in skeletal tissue are constantly sensing their environment and are quick to respond to injuries. Through new research published in Science Translational Medicine, they describe how this response profoundly affects growth plates, the soft cartilage at the end of bones in children that support normal growth and development, and how it responds to targeted treatment in mice.

Following a growth plate injury, a rapid invasion of nerve fibers and blood vessels triggers the formation of an unwanted “bony bar,” a rigid bone-like structure that can ultimately impede recovery and lead to stunted or altered bone growth. Through this new research, the team found inhibiting TrkA+ sensory neurons with long-acting bupivacaine, an FDA-approved nerve-numbing anesthetic, reduced this abnormal growth by up to 60%.