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UCLA Biologists Slow Aging, Extend Lifespan of Fruit Flies

저자:   업로드:2017-09-07  조회수:

    UCLA scientists working with middle-aged fruit flies say they were able to improve the insects' health while significantly slowing down their aging process. The team thinks its technique could eventually lead a way to delay the onset of Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, and other age-related diseases in humans.


    The researchers zeroed in on mitochondria, which often become damaged with age. When cells can't eliminate the damaged mitochondria, they can become toxic and contribute to a wide range of age-related diseases, said David Walker, Ph.D., a UCLA professor of integrative biology and physiology, and the study's senior author.


    Dr. Walker and his colleagues found that as fruit flies reach middle age—about one month into their two-month lifespan—their mitochondria change from their original small, round shape.


    "We think the fact that the mitochondria become larger and elongated impairs the cell's ability to clear the damaged mitochondria," he said. "And our research suggests dysfunctional mitochondria accumulate with age, rather than being discarded."


    The study ("Promoting Drp1-Mediated Mitochondrial Fission in Midlife Prolongs Healthy Lifespan of Drosophila melanogaster"), published in Nature Communications, reports that the UCLA scientists removed the damaged mitochondria by breaking up enlarged mitochondria into smaller pieces and that when they did, the flies became more active and more energetic and had more endurance. Following the treatment, female flies lived 20% longer than their typical lifespan, while males lived 12% longer, on average. The research highlights the importance of the protein Drp1 in aging, at least in flies and mice, where levels of Drp1 drop with age.




    "We find that short-term induction of Drp1, in midlife, is sufficient to improve organismal health and prolong lifespan, and observe a midlife shift toward a more elongated mitochondrial morphology, which is linked to the accumulation of dysfunctional mitochondria in aged flight muscle. Promoting Drp1-mediated mitochondrial fission, in midlife, facilitates mitophagy and improves both mitochondrial respiratory function and proteostasis in aged flies," write the investigators.


    "Finally, we show that autophagy is required for the anti-aging effects of midlife Drp1-mediated mitochondrial fission. Our findings indicate that interventions that promote mitochondrial fission could delay the onset of pathology and mortality in mammals when applied in midlife."

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