Scientists identify anti-aging enzyme for longevity and healthy life

At some point in our lives, we all might have thought of living a life that is longer than expected. Some of us may have spent hours researching the secret to longevity. Now, science, as usual, comes to our aid.

Eyleen Jorgelina O'Rourke of the University of Virginia and her colleagues are on a mission to discover mechanisms that not only extend life but also promote healthy aging. And their labor of hard work is finally paying off. The researchers discovered an enzyme that may slow the aging process. 

Interestingly, the enzyme eliminates ethanol — the common alcohol found in beer — from our bodies. The statement highlights that the enzyme has previously been well-studied, which may bring us closer to finding drug solutions sooner.

The road to finding the body's underlying mechanisms

To discover the secrets of anti-aging, the researchers studied something unusual — microscopic worms called Caenorhabditis elegans (C. elegans). Surprisingly, these soil dwellers and our genes have 70 percent in common, making them excellent candidates. In fact, they were the study model for two Nobel prizes-winning discoveries in medicine.

While studying worms, they identified a mechanism named "Alcohol and aldehyde-dehydrogenase Mediated Anti-aging Response." The team reveals it is shortened to AMAR, which translates to immortality in the Sanskrit language. "We went after a very well-supported hypothesis that the secret to longevity was the activation of a cell-rejuvenating process named autophagy and ended up finding an unrecognized mechanism of health and lifespan extension," said O'Rourke. 

This anti-aging mechanism works by activating a specific gene called adh-1. Through this process, the gene was able to produce more alcohol dehydrogenase (enzyme), thereby removing the body's toxic by-products of fat, namely glycerol, and glyceraldehyde. These by-products build up over time as we age. As a result, health complications arise. 

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.

Study abstract:

Several molecules can extend healthspan 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. Toward this goal, we searched for effectors acting downstream of the transcription factor EB (TFEB), known as HLH-30 in C. elegans, because 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.