Following the experiment, the worms lived 50 percent longer as well as displayed healthier signs.
To be certain, they tested the AMAR mechanism on another lab model: yeast. This single-celled microorganism shares a common genetic makeup with humans. And came up with similar results.
“We hope to attract interest in developing therapeutics that target AMAR,” said O’Rourke. She concluded by adding, “With age-related diseases currently being the major health burden for patients, their families, and the healthcare system, targeting the process of aging itself would be the most effective way to reduce this burden and increase the number of years of independent, healthy living for all of us.”
The results have been published in the journal Current Biology.
Several molecules can extend health span and lifespan across organisms. However, most are upstream signaling hubs or transcription factors orchestrating complex anti-aging programs. Therefore, these molecules point to but do not reveal the fundamental mechanisms driving longevity. Instead, downstream effectors that are necessary and sufficient to promote longevity across conditions or organisms may reveal the fundamental anti-aging drivers. Towards this goal, we searched for effectors acting downstream of the transcription factor EB (TFEB), known as HLH-30 in C. elegansbecause TFEB/HLH-30 is necessary across anti-aging interventions and its overexpression is sufficient to extend C. elegans lifespan and reduce biomarkers of aging in mammals including humans. As a result, we present an alcohol-dehydrogenase-mediated anti-aging response (AMAR) that is essential for C. elegans longevity driven by HLH-30 overexpression, caloric restriction, mTOR inhibition, and insulin-signaling deficiency.