'Stop-the-Clock' Gene That Delays Ageing and Increases Lifespan by 30% Discovered
Scientists at UCLA have identified a gene that can help slow the ageing process throughout the entire body when activated remotely in one of the key organs.
This could help medical treatment intervene in one stroke to delay many ageing-related diseases like Alzheimer's, Parkinson's, stroke, cardiovascular problems, etc.
By increasing the amount of the gene AMPK in fruit flies' intestines, they were able to increase the lifespan by 30%. More important, the ageing process applied to all key organs, thus ensuring an overall healthy lifespan.
The gene is a key energy sensor in cells that is activated when cellular energy levels go low.
Humans too have the gene, though it is usually not activated.
Many neurodegenerative diseases like Alzheimer's and Parkinson's are associated with the accumulation of cellular garbage in the brain resulting from old or damaged cells being discarded.
The team studied the role of AMPK in this process of 'garbage clearance' by checking if activating the gene led to accelerated rates of clearance.
What they saw was that activation of the gene in the nervous system led to increased levels of garbage clearance not only in the brain but also the intestine, proving its pan-organ influence.
The research, published on September 4 in the open-source journal Cell Reports, could have important implications for delaying aging and disease in humans, said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.
"We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated," Walker said.
In research published last year, Walker and his colleagues had identified another gene, called parkin that delayed the onset of aging and extended the healthy life span of fruit flies. The gene marks damaged proteins so that cells can discard them and also aids in the removal of damaged mitochondria from cells.
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