Is there really a cure for ageing? Scientists discover breakthrough procedure to replace specific parts of ageing cells by getting them to eat themselves to death.
• As we age, our mitochondrial DNA mutates, deteriorating and eventually killing off cells
• Mitochondria are inefficient naturally repairing mutations
• Scientists at Caltech and UCLA have developed a way to trigger mitochondria to clear out mutated genes
• So far its worked on flies but like may pave the way for age-halting ops on human
A landmark study has identified a new way to replace ageing cells in our body.
The research by scientists at Caltech and UCLA could pave the way to developing nip-n-tuck style procedures that reverse and slow the ageing process.
The experiment targeted mutated DNA inside our mitochondria – the ‘battery’ of our cells. As we age, our DNA breaks down and mutates. But unlike other parts of the body, the mitochondria are not very good at repairing DNA.
But now, in a groundbreaking procedure, the Caltech-UCLA team has found a way to manipulate genes so that they break down and remove mutated DNA, regenerating the cells.
The operation is a twist on an already-documented natural procedure called autophagy (‘self-eating’). As a result of autophagy, cells can digest dysfunctional mitochondria, clearing the way for healthy replacements.Research into autophagy that earned a Nobel Prize this year.But prior to the Caltech-UCLA it has not been clear whether this process could also promote the selective elimination of mutant or ageing DNA.
The accumulation of mutant mtDNA over a lifetime is thought to contribute to aging and degenerative diseases of aging such as Alzheimer’s, Parkinson’s, and sarcopenia— age-related muscle loss and frailty.Inherited defects in mtDNA are also linked to a number of conditions found in children, including autism.
To test their method, the team used a common fruit fly.
They focused on mitochondrial DNA in the muscles it uses to fly, since this is one of the most energy-draining tissues in the animal kingdom.
Like in humans, fruit flies’ muscles show some of the clearest signs of ageing.
Fruit flies and humans are share many disease genes.
In the experiment, the fruit fly was genetically engineered so that 75 percent of its mtDNA was mutated early on.
They then artificially increased the activity of genes that promote mitophagy.
In doing so, the fraction of mutated mtDNA in the fly muscle cells was dramatically reduced.
One gene in particular – called ‘parkin’ – reduced the fraction of mutant mtDNA from 76 percent to 5 percent when it was overexpressed.
Our goal is to create a future in which we can periodically undergo a cellular housecleaning to remove damaged mtDNA from the brain, muscle, and other tissues
Bruce Hay, Caltech professor of biology and biological engineering
Another gene – called ‘Atg1’ – reduced the fraction to 4 percent.
These are both genes which seem to be underactive in elderly people and people with degenerative diseases like Parkinson’s.
‘Such a decrease would completely eliminate any metabolic defects in these cells, essentially restoring them to a more youthful, energy-producing state,’ Professor Hay said.
‘The experiments serve as a clear demonstration that the level of mutant mtDNA can be reduced in cells by gently tweaking normal cellular processes.’
He added: ‘Our goal is to create a future in which we can periodically undergo a cellular housecleaning to remove damaged mtDNA from the brain, muscle, and other tissues.
‘This will help us maintain our intellectual abilities, mobility, and support healthy aging more generally.’