Mid-life modifications of mitochondrial fission/fusion that slow aging: molecular mechanisms to pharmacological treatments
Healthy mitochondria—the tiny “power plants of the cell”—are critical to the proper function of our cells, tissues, and organs. But with age, our cells accumulate damaged mitochondria. This accumulation has been implicated in numerous age-related diseases and may contribute to poor health associated with getting older.
Dr. Walker and his team have discovered that activating genes involved in the removal of defective mitochondria can slow the aging process and prolong the healthy lifespan of fruit flies. Importantly, some of these interventions only need to be applied for a short period of time to middle-aged animals in order to see future health benefits.
Dr. Walker’s lab is now working to better understand the cellular mechanisms at play. The group hopes to identify drugs that can mimic the anti-aging effects of these mid-life interventions, both at a cellular and organismal level. Such pharmacological agents could prolong the period of life spent in good health by delaying the onset and/or slowing the progression of age-related diseases such as cancer and Alzheimer’s disease. To achieve that goal, the team will expand its research program beyond invertebrate models, such as fruit flies, to include work in mammalian cells.