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Over the 20th and 21st centuries the average lifespan of human beings across the world has been getting longer and longer, but interestingly this rarely correlates with an increase in healthspan, meaning the period of a human life where age-related physiological and neurological decline hasn’t impeded the individual’s ability to live healthy and happily.

In fact, the two can be clearly dissociated from one another, and it’s possible for a human being to live a long and substantially unhealthy life. A policy framework and ageing literature review published in 2016 in the journal Lancet found that “evidence that increasing longevity is being accompanied by an extended period of good health is scarce”.

This presents the growing number of scientists looking to slow down, prevent, or even reverse the process of aging with a challenge of identifying the negative age-related epigenetic behaviors as well as positive behaviors in old people.

Now a new paper published in Nature from the University of Shanghai demonstrates a conserved epigenetic mechanism which underlies healthy aging in the brain and mitochondria elsewhere.

Healthy aging

RNA is the molecule which reads our DNA – kind of like the laser on a CD player, or the needle on your turntable. The scientists used a method called genome-wide RNA-use screening, where they examined the interactions between RNA and with genes that regulate cell behavior deterioration in C. elegans, a kind of worm used standardly for scientific research.

Among 59 potential culprits their screening identified, there were 2 epigenetic regulators (proteins which regulate gene-expression which were found to be associated with age-related behavioral decline in not just the C. elegans, but elderly mice, and even human cells.

The manner in which the regulators in question interfere with healthy aging is by repressing the expression of nuclear-encoded mitochondrial proteins, meaning the proteins needed to maintain mitochondria cannot be produced when the identified regulators were expressing themselves.

These proteins are coded in our DNA, and just like if there are scratches on the surface of your CD, the laser can’t read it and the music skips, the regulators express themselves in such a way as to prevent RNA and other genes from identifying the codes to build the proteins the mitochondria need.

In humans, the expression of the two corresponding epigenetic regulators (though slightly different to the ones in the C. elegans) in the frontal cortex was associated with Alzheimer’s disease.

In elderly mice, the surgical removal of one these regulators prevented age-related body-weight gain as well as cognitive decline.

These findings uncover a molecular mechanism that underlies mitochondrial dysfunction during ageing, and it is the identification of these genetic functions which is drawing scientists ever nearer to understanding the large puzzle pieces of why we decline as we age, and how we can prevent this.