Scientists Slow Aging in Flies Through Activation of AMPK gene. But that’s not all.
It’s been known for nearly a decade that AMPK (AMP-activated protein kinase) plays a role in regulating the lifespan of organisms. Scientists previously showed that increased levels of the protein produced by the AMPK gene dramatically increased the lifespan in the common worm model Caenorhabditis elegans (C. elegans).
Slightly more recent studies have shown that AMPK is a necessary component of the much reported and relatively controversial benefits of dietary restriction, which itself has been shown to increase lifespan.
Now scientists at the University of California, Los Angeles and the Université Paris Diderot have shown, quite amazingly, that the effects of increased AMPK activity need not be organism-wide to see organism-wide benefits.
In other words, increasing the activity of the AMPK gene in only one cell-type of the body gives anti-aging benefits throughout the entire organism. Scientists call this phenomenon cellular non-autonomy.
In the study published in Cell Reports, researchers introduced a special form of the AMPK gene into the model organism Drosophila melanogaster (more commonly known as the fruit fly). The researchers could activate the special gene “remotely” by feeding the flies a steroid compound known as RU-486. They found that by introducing and activating AMPK in either the flies’ intestines or their neurons the flies enjoyed a longer lifespan.
The life extending benefits of the AMPK gene are thought by the researchers to be effective through increased autophagy, otherwise known as cellular recycling. From the study:
Although AMPK, a key regulator of autophagy, has also been linked to aging and lifespan determination, little was known about the relationships between AMPK and autophagy in the coordination of tissue and organismal aging. In this study, we show that adult onset upregulation of AMPK in either the nervous system or intestine stimulates autophagy in the target tissue and is sufficient to prolong Drosophila lifespan.
Furthermore the whole-body effects of increased AMPK activation may have to do with decreased insulin-like signaling in the body. Although the exact link between the two is yet to be seen. Again, from the study:
[…] these findings suggest that the whole-body effects associated with localized AMPK/Atg1 upregulation may be mediated by altered DILP (Drosophila insulin-like peptide) signaling.
Taken together these results show great promise towards one day permanently slowing the aging process in humans, without the potentially dangerous (and difficult) need to change the entire organism’s genome.
Those interested in reading the study can find it here