RESTOR­ING YOUTH

Harper’s Bazaar (Malaysia) - - The Beauty -

The prob­lem be­gins with the fact that our cells, like our­selves, have a fi­nite life span. Af­ter di­vid­ing about 50 times, many types of cells reach the Hayflick limit, where they sim­ply run out of gas and quit mul­ti­ply­ing. This, it’s long been thought, is why we lose our abil­ity to re­gen­er­ate and heal: Things sag, bag, and go ka­put.

But more re­cently, sci­en­tists have re­alised that the real prob­lem is what those cells do af­ter they’re done di­vid­ing. At that point, they can en­ter a senes­cent state, where they’re ba­si­cally re­tired but not dead. Rather than just sit­ting there qui­etly, how­ever, senes­cent cells can spew out a toxic brew of in­flam­ma­tory fac­tors that poi­sons the cells around them. Some re­searchers be­lieve they could be partly re­spon­si­ble for some of the aspects of age­ing – ev­ery­thing from cataracts to can­cer.

“Senes­cent cells are clearly bad and con­trib­ute to the age­ing process,” says Laura Niedern­hofer, a DNA re­searcher at the Scripps In­sti­tute in Jupiter, Florida. “So there’s been a race to find drugs that can tar­get them.”

Lately, the race took a huge leap for­ward. A study co-au­thored by Niedern­hofer showed that two rel­a­tively well-known com­pounds ap­peared to kill senes­cent cells in mice while leav­ing nor­mal cells in­tact. Pre­vi­ously, senes­cent cells had been thought to be hard to iso­late and purge. But in mice whose mus­cles had been pre­ma­turely aged by ra­di­a­tion, the com­bi­na­tion was shown to re­store their youth­ful spring. El­derly mice on the same treat­ment ex­pe­ri­enced im­proved heart func­tion. Even bet­ter, both com­pounds have al­ready been cleared for other uses: Dasa­tinib is an FDA-ap­proved leukaemia drug, and quercetin is a com­mon an­tiox­i­dant flavonoid sold as a sup­ple­ment that is found in, among other things, cilantro, onions, ca­pers, and, of course, kale.

In other stud­ies, zap­ping senes­cent cells has also been shown to stem the loss of sub­cu­ta­neous fat, a “good” kind of fat that makes skin ap­pear smooth but that we lose with age. “We hope that clear­ing senes­cent cells will have wide­spread health ben­e­fits,” says Ju­dith Camp­isi, a cell and molec­u­lar bi­ol­o­gist at the Buck In­sti­tute for Re­search on Ag­ing in Marin County, Cal­i­for­nia, who has stud­ied cells senes­cence for more than two decades. Ac­cord­ing to Camp­isi, those ben­e­fits may in­clude pre­vent­ing ath­er­o­scle­ro­sis, os­teoarthri­tis, some can­cers, and Parkin­son’s dis­ease – and sev­eral other senes­cent-clear­ing drugs are be­ing stud­ied.

Clin­i­cal tri­als are al­ready be­ing planned for the dasa­tinib-quercetin com­bi­na­tion, but study se­nior au­thor James Kirk­land, di­rec­tor of the Robert and Ar­lene Ko­god Cen­ter on Ag­ing at the Mayo Clinic in Rochester, Min­nesota, warns that it’s too soon for peo­ple to use them be­cause of the un­known side ef­fects.

EX­ER­CISE IN A PILL?

An­other trou­ble spot in our cells is the mi­to­chon­dria, the tiny cel­lu­lar en­ergy plants that con­vert nu­tri­ents to fuel. As we get older, mi­to­chon­dria lose their abil­ity to func­tion – per­haps con­tribut­ing to cell senes­cence – but sci­en­tists have long noted that ex­er­cis­ing seems to help keep them in tune. A team at the Univer­sity of South­ern Cal­i­for­nia Leonard Davis School of Geron­tol­ogy iden­ti­fied a pep­tide pro­duced in the mi­to­chon­dria that ap­pears to mimic many of the ben­e­fits of ex­er­cise, such as im­proved me­tab­o­lism and in­creased in­sulin sen­si­tiv­ity; mice who were in­jected did not be­come obese, de­spite eat­ing all they wanted.

“It acts like ex­er­cise; that’s very clear,” says study se­nior au­thor Pin­chas Co­hen of the pep­tide, called MOTS-c. “It in­creases en­ergy ex­pen­di­ture, which is what we mea­sured.” But, he cau­tions, any “ex­er­cise pill” is at least five years away – which means you still have to hit the gym, for now.

Newspapers in English

Newspapers from Malaysia

© PressReader. All rights reserved.