Longevity researcher is yielding important pieces of the puzzle that is senescence, like what role faulty protein production plays
30s are the new 20s… 50s are the new 40s… Every now and then, a spare pundit somewhere—fashion, career advice, matrimonial services(?)—mouths/types trite sentences like these, hoping to nudge a total reset of aspirations, of behaviour. At the very least, one would suspect, all of it would be oriented towards legitimising something that you were perhaps wondering was appropriate for your age cohort or not. Underneath the cliché lies the recognition of the desire to be young for longer. But, what is “being young”? If you were the average Indian guy in 1960, you would have died before turning 45. Would you have thought of your 30s as your prime then?
Such releative perception of age and time makes it difficult to imagine the 70s, even 80s, being the new 40s—50s at the worst. Is it really possible? Well,there is certainly a lot of money being poured into ageing and longevity research. There are big backers—last year, Switzerland-based Korify Capital committed $100 million to such research. One of the richest men on the planet, Jeff Bezos, has backed Altos Labs, which is reportedly working on cell rejuvenation, a fundamental premise of any longevity goal. These are only two in a fairly large pool of longevity-research investment. To get to beating ageing, we have to of course understand why and how organisms age.
The findings of a study published in Science Advances finds a clue to this and thereby brings us closer to understanding how we can slowdown/stop, or even reverse, ageing. University of Zurich researchers show, through mice studies, how faulty protein production could hasten ageing. Errors of translation of genetic messages from the nucleus, at the site of protein-production (the ribosomes, cell organelles that read these messages and align amino acids in specific sequences in response), cause the resulting proteins to ‘fold’ in manner that makes them injurious to cells
The Zurich researchers tweaked mice genes to make their ribosomes more prone to errors than usual. In their initial years, the modified mice seemed as healthy as their control-set counter-parts. Nine months post birth, they were looking and acting much older in comparison to the control mice—with ailments tyical of ageing in mice, including slower movement. At the cellular level also, there were tell-tale signs of advanced age, from drastically eroded telomeres to molecules resulting from impaired metabolism, a common ageing feature. Then, of course, was the drastically shortened lifespan.
How many such blocks of knowledge will lead to build a full understanding of ageing, is hard to tell. But, a new array of tools—from emerging technology across fields—will likely give research warp-speed, in key areas, including genomics, proteomics and pathology. Pieces of the gargantuan puzzle that curing ageing likely is are getting churned out at a faster kip than before, from research on cell senescence, the role of telomeres, etc. Existing drugs are finding new purpose. Printed and laboratory developed organs, gene-editing technologies—all promise to put the fruit of longevity within our reach.