Biology

How hardy volcanic microbes helped track down an anti-aging "superhero" protein

How hardy volcanic microbes helped track down an anti-aging "superhero" protein
Hardy microbes that make their home in volcanic pools may hold the key to a new anti-aging drug
Hardy microbes that make their home in volcanic pools may hold the key to a new anti-aging drug
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Professors Ken O'Byrne (left) and Derek Richard are developing an anti-aging drug
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Professors Ken O'Byrne (left) and Derek Richard are developing an anti-aging drug
Hardy microbes that make their home in volcanic pools may hold the key to a new anti-aging drug
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Hardy microbes that make their home in volcanic pools may hold the key to a new anti-aging drug

A team of scientists, looking to figure out how hardy little creatures known as archaea thrive in boiling, volcanic pools of sulfuric acid like they were hot tubs, may have uncovered the key to an anti-aging drug. By manipulating a so-called "super hero" protein common to both archaea and humans, the researchers found a way to "trick" cells into acting younger by keeping the DNA repairing process running much longer than usual.

In previous studies, the researchers examined how archaea have managed to survive in such harsh conditions for billions of years. Eventually they determined that a protein called ssB1 was responsible by helping the organisms repair damage to their DNA. The team says the real eureka moment came when they discovered that we humans have our own versions of this protein, hSSB1.

"In normal cells, ssB1 is like a guardian angel that is looking after the genetic code and, if there is any damage, we see it rush in to repair that damage," says Derek Richard, co-author of the study. "But, as we age, we lose parts of our genetic code, and that is the foundation for diseases such as cancer and Alzheimer's. When we found that ssB1 was helping the archaea to repair its damaged DNA, we realized we might have stumbled across the basis for a new cellular treatment for humans, to control our aging pathway and keep people healthier, for longer."

The researchers examined how hSSB1 functions in humans, and discovered it works through a pathway that seems to control aging. The team found that as we get older our bodies down-regulate hSSB1 and related proteins, which slows down the DNA repair process, leading to a whole range of health problems.

"The big link between cancer and aging is DNA repair," says Ken O'Byrne, co-author of the study. "As we age, our target protein starts to function differently and allows our genome to be damaged and this damage can cause cancer."

Professors Ken O'Byrne (left) and Derek Richard are developing an anti-aging drug
Professors Ken O'Byrne (left) and Derek Richard are developing an anti-aging drug

The new drug works to restore the activity of hSSB1, preventing the DNA repair process from being shut down in the first place. That means cells continue to function as though they were much younger, effectively delaying or preventing the onset of various age-related health problems, such as cancer, Alzheimer's, diabetes and arthritis.

The researchers say the goal isn't to extend our lifespan, but improve our healthspan – the amount of our lives we spend in good health. The team is currently looking to raise more money to fund future development, including toxicology studies and, hopefully, eventual human trials.

The research was published in the journal DNA Repair, and the team describes the work in the video below.

Source: Queensland University of Technology

Interview with Assoc Prof Derek Richard

3 comments
3 comments
guzmanchinky
I'm 47. Hurry up.
HoppyHopkins
If they think the 47 year old is in a hurry, I am 64 and have early macular degeneration plus arthritis. I really could use a boost to my cellular repair system
Jim B
The SENS Foundation would suggest that this research is "messing with metabolism" and unlikely to produce gains in healthspan and lifespan in the near term. The real focus should be on removing the damage that causes aging and causes hSSB1 expression to fall.
Also a note to Michael Irving, you're probably already aware of this, but when researchers talk about extending "healthspan rather than lifespan" they of course know that it is impossible to extend healthspan without also extending lifespan, as people die from being sick, not from 'aging'. Until fairly recently it was an instant third rail of death for a researchers funding if they talked about extending lifespan, as for various reasons such as the pro aging trance the public saw this as impossible.