Anti-aging research is series focus

August 6, 2018  21:30

How close is medicine to an anti-aging pill? Can anti-aging therapies delay the onset of age-related degenerative diseases? What lifestyle choices can individuals make to prolong healthy lifespan?

These are some of the questions that will be addressed in a lecture series set for Aug. 6 to 10 at the MDI Biological Laboratory. Each of the lectures will be held at 4 p.m. in the Maren Auditorium.

David Sinclair will give the Kinter Lecture Monday, Aug. 6, on “Why Reversing Aging is Easier than Reversing Baldness.” Next, Judith Campisi will address “Aging and Cancer: Rival Demons?” Thursday, Aug. 6, in the Cserr Lecture. The Orland Lecture, Friday, Aug. 10, will be given by Heinrich Jasper. He will speak on “Finding Rejuvenating Interventions: Immunity and Stem Cells.”

The lecture series is part of a two-week course, “Comparative and Experimental Approaches to Aging Biology Research” being held at the institution.

“Medicine has traditionally tackled degenerative diseases on a disease-by-disease basis,” said course Director Aric Rogers, Ph.D. “But since the common risk factor is old age, an increased understanding of the biology of aging means that a single medicine may be able to address many of these diseases at once.”

“The average American lifespan has increased dramatically since 1900, but health hasn’t kept pace,” event organizers said in a statement. “About two-thirds of older Americans suffer from multiple age-related degenerative diseases, including Alzheimer’s, cancer, diabetes, heart disease and Parkinson’s.

“Recent research, including studies at the MDI Biological Laboratory, is finding that the cellular pathways that control aging also regulate age-related degenerative diseases, raising the prospect that anti-aging therapies can extend the healthy, productive years of middle age right up until the end of life.”

Sinclair is a professor at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biology of Aging. The goal of his work is to establish new biological approaches that can be translated into radically different medicines to promote longer, more productive lives. He is especially interested in how genetic and epigenetic changes drive aging, common diseases and disorders such as cancer, heart disease, inflammation, neurodegeneration, infertility and diabetes. Another interest is sirtuins, a family of proteins that is a key regulator of longevity.

Sinclair is the co-founder of several biotech companies. He is also co-founder and co-chief editor of the journal Aging. His work has been featured in books and documentaries and on television shows, including “60 Minutes.” He is an inventor on more than 40 patents and was listed by Time as one of the “100 most influential people in the world.”

Campisi’s research considers the genetic, environmental and evolutionary forces that lead to aging and age-related diseases with the aim of identifying pathways that can be modified to mitigate basic aging processes.

Her work has made significant contributions to understanding why aging is the largest single risk factor for cancer. She is recognized for her work on senescent cells—older cells that have stopped dividing—and their influence on aging and cancer. She joined the Lawrence Berkeley National Laboratory as a senior scientist in 1991 and established a second laboratory at the Buck Institute for Research on Aging in 2002.

Jasper heads a laboratory in the Immunology Discovery group at Genentech, where he studies the pathways and processes involved in a wide range of age-related inflammatory and degenerative diseases. His research is focused on the age-related decline of stem cell function and regenerative potential. His research has addressed whether the aging process can be influenced by optimizing stem cell activity.

Jasper is also a professor at the Buck Institute for Research on Aging, where his current projects focus on the role of insulin and stress signaling pathways in the control of tissue regeneration, metabolic homeostasis and cell death.

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