Scientists have identified a protein that switches brain aging on and off in mice. The findings were published in Nature Aging and may pave the way for new treatments for cognitive decline.
Knowing more about the cellular and molecular mechanisms behind age-related cognitive decline is key for finding new treatments that restore cognition in old age. In the current study, researchers set out to find pro-aging neuronal factors that could one day be used for reversing cognitive decline.
To do so, they examined how the genes and proteins in the hippocampus change in mice as they age. They identified one protein that differed between young and old animals: ferritin light chain 1 (FTL1)- an iron-associated protein. Old mice had higher levels of FTL1 as well as fewer connections between hippocampal neurons and reduced cognitive abilities.
The researchers conducted a series of experiments to understand more about FTL1’s effects. In one experiment, they artificially increased its levels in young mice, causing their brains and behavior to resemble those of older mice.
In another experiment, the researchers reduced levels of FTL1 in the hippocampi of old mice, causing them to resemble those of younger mice; developing more nerve connections and performing better in memory tests.
A petri dish experiment found that nerve cells engineered to produce high quantities of FTL1 grew simple, one-armed neurites as opposed to the branching neurites produced by normal cells.
"It is truly a reversal of impairments. It's much more than merely delaying or preventing symptoms," said senior author of the study, Saul Villeda, PhD, associate director of the Bakar Aging Research Institute at the University of California, San Francisco, in a press release.
"We're seeing more opportunities to alleviate the worst consequences of old age. It's a hopeful time to be working on the biology of aging,” he added.
Sources: Science Daily, Nature Aging