Telomeres are caps at the end of DNA that protect our chromosomes, similar to the plastic tips that prevent the ends of shoelaces from fraying. As we grow older, our telomeres shorten. It has been hypothesized that telomerase, the enzyme that maintains telomeres, could be used as an anti-aging therapy. However, in the first ever large-scale study of epigenetic aging rates among nearly 10,000 people, Horvath and his colleagues found an unexpected and paradoxical connection between the two aging clocks. Variants in a sub-unit of telomerase called TERT, are actually associated with faster epigenetic aging rates.

“This finding was quite surprising because there previously was no indication that a correlation existed between intrinsic epigenetic aging and telomere length,” said Steve Horvath, Ph.D. Professor in the Departments of Human Genetics and Biostatistics at the University of California, Los Angeles. “Given the recognized significance of telomere shortening and epigenetic aging, it is intellectually satisfying that our study links these two recognized aging clocks even though the link is opposite of what one would expect.”

Horvath is a two-time Allen Distinguished Investigator. His current project is focused on developing a universal epigenetic aging clock to measure aging across different species.

“This pioneering discovery has arisen because of Steve’s commitment to the frontiers of aging – and this novel control system for the aging clock may also open new paths to multiple diseases of aging including neurodegeneration, which have resisted traditional approaches,” said Tom Skalak, Executive Director of The Paul G. Allen Frontiers Group.