Acrossing the evolutionary spectrum, ageing appears universal but complex. Research of ageing is aim to unerstand, slow, stop and/ or reverse its process. Going simple is the new exciting. For instance, whether single gene may control ageing? Around twenty years ago, “many, not single gene”, probably most answers you may heard. However, for the first time, surprisingly biochemist genius Dr. Cynthia Kenyon was able to prove that a simple genetic mutation Daf-2/IGF1 caused a simple worm, Caenorhabditis elegans (C. elegans) to double the lifespan.

Moreover, ten years ago, in lab described that deficiency of single protein kinase termed “the target of rapamycin” (TOR) may double its life span in C. elegans too. Interestingly, long– lived mutants are resistant to many ageing-related diseases and bacterial infection. One latest study agrees that there might be some universal mechanisms for activating anti-aging pathway, i.e., single molecule that treats multiple age-related diseases, for example, SIRT1, yet controversy is not completely resolved. Thus some “drivers” for ageing may exist; even it need eventually dictate a defined group of genes via its cascade. Lifespan in model organisms appears plastic and subjected to modulation of genetic, nutritional or pharmacological intervention . Thus we might significantly extend youthful human life through understanding of the influence that genetics have on age-related diseases (from cancer, ND, OA , diabetes to heart failure) in living things.

Remarkably, if we can extrapolate from the adult lifespan in age1(mg44) (i.e.AGEing alteration) animals relative to its control wild type nematode C. elegans, we may live extremely long lives, and up to 1000 years. It is always tantalizing to discover the “fountain of youth”. Indeed, countless men tried this or that way to avoid ageing, from Babylonian epic of Gilgamesh, to Poncede Leon, as well as Emperor Chin in chin Dynasty in China sending out 300 young boys sailing to Pacific sea to seek for “the elixir pill”. Of certain, a long distance remains to translate from insights gained in animal models to human beings! A better understanding of the targets of such interventions, as well as the proximate causes of ageing-related degeneration and disease, is critical for the evaluation in abrogation of human senescence.

It is essential to better understand the molecular pathways underpinning the ageing process, with this knowledge to obtain novel therapeutic strategies to treat ARDs. In general, some interventions could be two-sided swords. However, we may hypothesize, by modulating the natural machinery; there is a huge room to explore new health benefical windows in cellular processes. With a cost, the modulation or reversal of ageing and ARD emerge through modulation of mTOR and beyond, such as telomere.

Regards
John George
Journal of Aging Science