Mitochondria And Aging: Fruit Flies...And Perhaps Humans As Well

By André Karwath aka Aka - Own work, CC BY-SA 2.5, https://commons.wikimedia.org/w/index.php?curid=227170

The mitochondria are the “powerhouses” of the cell, and problems with mitochondria and mitochondrial function have been associated with a number of diseases and disorders. Increased levels of dysfunctional mitochondria have been linked to aging, and this study linked here shows that “middle-aged” Drosophila (fruit flies) tend to have more elongated, dysfunctional mitochondria. Upregulation if a gene called Drp-1 promotes fission of those aberrant mitochondria, which in turn enhances mitophagy (in simple terms: cellular “clean-up” of the dysfunctional mitochondria) and enhanced mitochondrial function.  This in turn has anti-aging effects in the flies. Now, the objective here is not to improve the health of aging fruit flies (which may or may not be a worthy goal on its own, depending on your perspective), but to apply these findings to the human case, and to see how further investigation into these findings can inform us about ant-aging strategies in humans. This is the basic science-human health link on full display.  Abstract:

The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is missing. Here, we show that upregulating Drp1-a Dynamin-related protein that promotes mitochondrial fission-in midlife, prolongs Drosophila lifespan and healthspan. 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. 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. Mitochondrial fission and fusion are important mechanisms to maintain mitochondrial function. Here, the authors report that middle-aged flies have more elongated, or 'hyper-fused' mitochondria, and show that induction of mitochondrial fission in midlife, but not in early life, extends the health and life of flies.