Scientists can reverse brain aging in fruit flies by preventing buildup of a common protein

Good news! My old brain already feels younger just reading about it! 😊

These results seem to be very promising!

More on discovering the fountain of youth!

"Key takeaways

• Buildup of a protein called filamentous actin, or F-actin, in the brain inhibits the removal of cellular wastes, including DNA, lipids, proteins and organelles.
• The resulting accumulation of waste diminishes neuronal functions and contributes to cognitive decline.
• By tweaking a few very specific genes in the neurons of aging fruit flies, the researchers prevented F-actin buildup, maintained cellular recycling and extended the healthy lifespan of fruit flies by approximately 30%.

...
when a common cell structural protein called filamentous actin, or F-actin, builds up in the brain, it inhibits a key process that removes unnecessary or dysfunctional components within cells, including DNA, lipids, proteins and organelles. The resulting accumulation of waste diminishes neuronal functions and contributes to cognitive decline. By tweaking a few specific genes in aging fruit flies’ neurons, the researchers prevented F-actin buildup, maintained cellular recycling and extended the healthy lifespan of fruit flies by approximately 30%. ...

Their first clue of a correlation: Flies on a restricted diet both lived longer and had less F-actin buildup in their brains.

Their second clue: When treated with a drug known to extend lifespan, called rapamycin, there was also less F-actin in the brains of aged flies. ...

“When we reduced Fhos expression in aging neurons, it prevented the accumulation of F-actin in the brain,” ...

Even though the genetic intervention was targeted to just neurons, it improved the flies’ overall health. They lived 25-30% longer, while showing signs of improved brain function as well as markers of improved health in other organ systems. ...

Further investigation showed the F-actin was interfering with the body’s “cellular garbage disposal system.” Damaged or superfluous proteins and other components inside a cell are broken down in a process called “autophagy.” Aging research has established that autophagy pathways become less active with age, but no one knew exactly why. ..."

From the abstract:

"The actin cytoskeleton is a key determinant of cell structure and homeostasis. However, possible tissue-specific changes to actin dynamics during aging, notably brain aging, are not understood. Here, we show that there is an age-related increase in filamentous actin (F-actin) in Drosophila brains, which is counteracted by prolongevity interventions. Critically, decreasing F-actin levels in aging neurons prevents age-onset cognitive decline and extends organismal healthspan. Mechanistically, we show that autophagy, a recycling process required for neuronal homeostasis, is disabled upon actin dysregulation in the aged brain. Remarkably, disrupting actin polymerization in aged animals with cytoskeletal drugs restores brain autophagy to youthful levels and reverses cellular hallmarks of brain aging. Finally, reducing F-actin levels in aging neurons slows brain aging and promotes healthspan in an autophagy-dependent manner. Our data identify excess actin polymerization as a hallmark of brain aging, which can be targeted to reverse brain aging phenotypes and prolong healthspan."

Scientists can reverse brain aging in fruit flies by preventing buildup of a common protein | UCLA

Accumulation of F-actin drives brain aging and limits healthspan in Drosophila (open access)

Fig. 1: F-actin accumulates in aged Drosophila brains and correlates with health.