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Scientists can now slow aging and extend lifespan

Cosmetic companies tout products that slow aging and provide a more youthful look, but no cosmetic can reverse the damaging effects of Parkinson’s, cardiovascular disease, cancer, and other diseases related to age decline. But now, new research from UCLA scientists found a way to slow aging and extend the healthy lifespan of fruit flies.

The key to the breakthrough was targeting mitochondria, the part of the cell in charge of growth and determining when the cell lives and dies.

The study was conducted by Anil Rana, lead author and UCLA project scientist, and David Walker, senior author and UCLA Professor of Integrative Biology and Physiology.

As we age, damaged mitochondria build up in the brain, muscles, and other organs. The stored up mitochondria are the cause of many age related health problems.

The researchers noticed that when fruit flies reach middle age, about a month into their typical two-month lifespan, their mitochondria starts to change shape, becoming thinner and more oblong.

“We think the fact that the mitochondria become larger and elongated impairs the cell’s ability to clear the damaged mitochondria, and our research suggests dysfunctional mitochondria accumulate with age, rather than being discarded,” said Walker.

Walker and his colleagues removed the damaged mitochondria in fruit flies using two different methods, and both resulted in the fruit flies living longer with a healthier lifespan.

For one method, the researchers increased Drp1 levels in the fruit flies. Drp1 is a protein vital to the aging process, and by increasing its levels, the researchers saw the long damaged mitochondria breaking up into smaller manageable pieces that were then discarded in the fruit flies.

Breaking up damaged mitochondria gave the fruit flies more energy and endurance and increased their lifespans.

In another method, researchers turned off a protein called Mfn, which stopped the damaged mitochondria from bonding together and turning into bigger pieces. This method also resulted in similar age slowing effects.

“You can either break up the mitochondria with Drp1 or prevent them from fusing by inactivating Mfn. Both have the same effect: making the mitochondrial smaller and extending lifespan,” said Rana.

Walker hopes this researcher can be extended to humans and effectively delay age related decline, halting the serious effects of age related diseases like Parkinson’s, cardiovascular disease, and cancer.

By Kay Vandette, Staff Writer

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