Scientists at UCSF’s Bakar Aging Research Institute examined activity in the hippocampus, the brain’s command center for learning and memory. Comparing young and old mice, the researchers discovered that older brains, unlike younger ones, were flooded with the FTL1 protein.
To figure out whether the protein was actually the culprit or just another byproduct of the aging process, they elevated FTL1 levels in young mice, whose brains soon began to look and act old. Their neurons quit branching out into complex networks, shrinking instead into stubby extensions that no longer communicated with the efficiency of youth.
But it was the next step in their experiment that ended in a revelation. Lowering the protein levels in older mice didn’t just slow or stop the fraying of the older brain. Clearing out the FTL1 clutter helped rebuild lost connections in the hippocampus and literally healed existing damage. The proof: The treated mice soon scored “significantly better” on memory tests.
“It is truly a reversal of impairments,” says Saul Villeda, PhD, the study’s senior author. “It’s much more than merely delaying or preventing symptoms.”
The groundbreaking study also revealed how the offending protein does its harm. Researchers learned that high levels of FTL1 act like a metabolic brake, slowing energy production within brain cells. When those cells are no longer able to power themselves, the connections between synapses soon ebb and dry up.
Someday soon, the good news for mice could be great news for humans. Medically approved treatment plans may be years away, but the new study does offer a more immediate reason for optimism: Brain drain associated with aging can now be credibly considered a manageable biological setback, not a permanent loss.
