Researchers at the University of California, San Francisco (UCSF) say they have successfully reversed memory loss in aging mice by targeting a specific protein that accumulates in brain cells.
They revealed that the finding could one day open new pathways for treating age-related cognitive decline.
The peer-reviewed study, published in Nature Aging, focused on a protein called ferritin light chain 1 (FTL1).
Scientists found that FTL1 levels rise in the brain’s memory center as mice age, impairing energy production and starving neurons of the power needed to store and form memories.
When researchers artificially increased FTL1 in young mice, the animals quickly developed memory problems, performing as poorly as older mice in maze and object-recognition tests.
But when they reduced FTL1 in older mice, the results were dramatic: their memory and learning abilities returned to levels seen in much younger animals.
“It is truly a reversal of impairments. It’s much more than merely delaying or preventing symptoms,” said Dr. Saul Villeda, associate director of the UCSF Bakar Aging Research Institute and senior author of the study.
The findings point researchers toward a broader approach to cognitive decline.
Until now, most dementia research has centered on the accumulation of amyloid plaques and tau tangles in the brain, hallmarks of Alzheimer’s disease.
But FTL1 offers a potential new target that could benefit a wider population.
Unlike Alzheimer’s, which affects only a portion of the elderly population, nearly all adults experience some degree of memory loss as they age.
Roughly 6–12 million Americans over 65 have been diagnosed with mild cognitive impairment, a condition that can progress to dementia.
The UCSF team says their work represents a step toward addressing the “general wear and tear” of aging on the brain, not just the extreme cases tied to neurodegenerative disease.
Using genetic tools and viral vectors, researchers manipulated FTL1 levels in the brains of mice.
They then measured brain energy output, iron storage, and the number of connections between neurons.
The results consistently showed that higher FTL1 correlated with weaker performance, while reducing it restored youthful cognitive function.
To ensure the results were valid, the experiments were repeated multiple times using different genetic approaches.
Each time, lowering FTL1 improved memory in the mice.
While the results have generated excitement, researchers caution against assuming the same outcome in humans.
The experiments were conducted only in male mice, and the human brain is far more complex.
Translating the findings into safe and effective treatments for people could take years.
Still, Villeda called the findings “a hopeful time to be working on the biology of aging,” noting that the research shows how new avenues may exist beyond the long-standing Alzheimer’s focus.
The study adds to growing evidence that the brain’s decline is not inevitable but potentially reversible.
By identifying proteins like FTL1 that interfere with neuron function, researchers may be able to develop treatments that slow, halt, or even reverse age-related memory loss in the wider population.
For millions of families dealing with cognitive decline and dementia, the UCSF findings provide a rare dose of optimism in a field where breakthroughs have been slow to come.
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