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Scientists at UCLA have conducted a study using fruit flies (Drosophila) to investigate the role of filamentous actin (F-actin) buildup in brain aging. F-actin is a common protein found in cells throughout the body that forms filaments essential for maintaining cell structure and various other functions. As fruit flies age, F-actin accumulates in their brains, which appears to inhibit autophagy, the process responsible for removing damaged or unnecessary cellular components. This accumulation of cellular waste leads to diminished neuronal function and cognitive decline, mirroring the effects of aging observed in humans.

The researchers observed a correlation between F-actin buildup and aging by examining flies on a restricted diet and flies treated with rapamycin, a drug known to extend lifespan. Both groups exhibited less F-actin accumulation and longer lifespans. To further investigate the causal relationship between F-actin buildup and aging, researchers genetically targeted and knocked down the Fhos gene in aging flies, a gene responsible for elongating and organizing actin filaments. This intervention successfully prevented F-actin accumulation in the flies' brains, resulting in improved overall health, including a 25-30% increase in lifespan, enhanced brain function, and positive health markers in other organ systems.

These findings strongly suggest that the buildup of F-actin is a driver of age-onset cognitive decline and that preventing this buildup can significantly improve healthspan, the period of life spent in good health. This discovery holds promise for developing interventions that could promote healthier aging in humans, although translating these findings to human applications presents challenges. Further research is needed to explore tissue-specific approaches for targeting actin polymerization in aged organisms. The ultimate goal of this research is to extend not only lifespan, but also healthspan, allowing individuals to enjoy a higher quality of life as they age.