2016—The First Biotech Company to Focus on Senescence Launches 

Senescence has emerged as one of the primary drivers of aging identified so far. In 2016 the Buck supported the launch of Unity Biotechnology, the first company to focus on translating the science of senescence to medicines designed to increase healthspan. The company, focused in large part on Buck science, was first located on our campus.

Near future—Targeting Aging with Metformin (TAME) Trial

This clinical trial, designed to test the hypothesis that the diabetes drug metformin can delay the onset of age-related disease, is the first clinical trial designed to target mechanisms of aging instead of a specific age-related condition. It aims to test 3,000 people aged 65-79 in 14 separate centers over 6 years to compare a wide range of health metrics between participants taking and not taking metformin.

2009—Rapamycin Extends Lifespan in Mice

Rapamycin is a drug used in humans to treat cancer and prevent organ rejection after transplantation. Rapamycin had already been known to extend average lifespan in invertebrate animals, such as fruit flies and roundworms. In 2009 it was reported that the drug can have similar effects in mice, suggesting that the effects might extend to other mammals, such as humans.

2007—The Field of Geroscience Established

As research into aging and age-related diseases continued to show increasing overlap, scientists at the Buck Institute named and fostered the emerging field of Geroscience via a prestigious “Breakthrough” award from the National Institutes of Health. Geroscience is the scientific field concerned with understanding the biological connection between getting older and the chronic diseases of aging.

2007—Exercise Reverses Muscle Aging

In another first for Buck science, the Melov lab showed that aging in humans can be reversed through exercise, specifically strength-training. The lab did genetic studies on muscle samples taken from both younger and older adults before and after a 6-month resistance training regimen. After training, the “genetic fingerprint” in the muscles of older adults had reverted to more closely resemble the genes active in the muscles of younger adults.

1988 & 1993—Genetic Mutations Increase Lifespan

Tom Johnson’s discovery in 1988 that a single genetic mutation, dubbed age-1, could increase the lifespan of the roundworm C. elegans by up to 65% catalyzed the modern era of research on aging. Further interest in the field was driven when Cynthia Kenyon published in 1993 that a mutation in the daf-2 gene doubled the worm lifespan. Research on age-1, daf-2, and other genes in their molecular network have led to profound discoveries about the role of nutrient signaling in aging, which forms one of the major pillars of the field.

1978 & 1985—Telomeres and Telomerase

Telomeres are protective sequences of DNA that sit at the tips of our chromosomes and have been compared to the caps at the end of shoestrings. They get shorter with age. Cells with critically short telomeres can no longer divide, making short telomeres a hallmark of aging. Elizabeth Blackburn made the discovery of telomeres in 1978, and in 1985 she discovered the enzyme telomerase, which can lengthen telomeres. She won the Nobel Prize for this work, which began in single-celled organisms called Tetrahymena thermophila, commonly known as pond scum.

1939—Caloric Restriction Increases Lifespan

The first study identifying a method to extend lifespan was published in 1939. This landmark study by McCay, Crowell, and Maynard found that caloric restriction (a diet that meets nutritional requirements but provides greatly reduced calories) in rats could increase their average lifespan. The biological mechanism of caloric restriction, and whether it works in humans, remains an important question in research on aging today.