A protein linked to the brain’s decline may be key to reversing memory loss and preventing diseases like Alzheimer’s, a new study says.
A growing body of research shows ageing is particularly harsh on the brain’s hippocampus, which is responsible for learning and memory. And ageing is the dominant risk factor for neurodegenerative disorders like Parkinson’s and Alzheimer’s.
The new study, published in the journal Nature Aging, concludes that a protein known as FTL1 is key to this decline.
Researchers found that old mice had more FTL1 as well as fewer connections between brain cells in the hippocampus and diminished cognitive abilities compared to younger mice.
When they artificially increased FTL1 levels in young mice, their brains and behaviour began to resemble that of old mice.
Lab-grown nerve cells engineered to make a large quantity of FTL1 grew fewer branches, the study noted.
“Here we identify ferritin light chain 1, an iron-associated protein, as a pro-aging neuronal factor that impairs cognition,” the researchers wrote in the study. “We detect an increase in neuronal FTL1 in the hippocampus of aged mice, the levels of which correlate with cognitive decline.”
When the amount of FTL1 in the hippocampus of old mice was reduced, they regained their youth. Such mice had more connections between nerve cells and did better on memory tests.
The researchers also observed that FTL1 slowed down metabolism in the cells of the hippocampus. But when these cells were treated with Nicotinamide Adenine Dinucleotide or NADH, an enzyme known to stimulate metabolism, it prevented these effects.
“Our data identify neuronal FTL1 as a key molecular mediator of cognitive rejuvenation,” the researchers wrote. “Our data raise the exciting possibility that the beneficial effects of targeting neuronal FTL1 at old age may extend more broadly, beyond cognitive aging, to neurodegenerative diseases in older people.”
The study noted that boosting metabolic functions with NADH supplementation mitigated the effects of ageing on cognition.
The researchers hope therapies developed to block the effects of FTL1 in the brain can lead to positive outcomes for dementia patients.
"It is truly a reversal of impairments,” Saul Villeda, a study author from the University of California San Francisco, said. "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 ageing.”
