SAN FRANCISCO, Aug 28: Researchers at the University of California, San Francisco (UCSF) have identified a key protein in the brain that could hold the potential to reverse age-related memory loss, marking a significant step forward in the study of cognitive decline and aging.

In a study published in the journal Nature Aging, scientists focused on a protein known as ferritin light chain 1 (FTL1). The research team found that elevated levels of FTL1 in brain cells were associated with cognitive decline, while reducing the protein in the hippocampus — the region responsible for memory and learning — led to improved neural connectivity and memory performance in mice.

“When we reduced FTL1 levels, the mice began to display brain characteristics and memory performance more commonly seen in younger animals,” said Dr. Saul Villeda, co-author of the study. “This is more than just slowing down symptoms — it's a reversal of impairments. It’s an exciting time to be researching the biology of aging.”

The team initially analyzed how gene and protein expressions changed in mice over time, leading them to identify FTL1 as a driver of neural aging. To confirm the protein’s role, scientists increased FTL1 in younger mice. The result: their mental performance began to resemble that of older animals, further reinforcing the protein’s significance.

In lab conditions, researchers observed that nerve cells exposed to higher FTL1 levels produced simpler neurites — the projections that connect neurons — instead of the complex, branched structures typically seen in healthy brain cells. This structural change is believed to contribute to diminished cognitive function.

The study also cited previous findings from 2015 that linked elevated ferritin in cerebrospinal fluid with cognitive decline and progression from mild cognitive impairment to Alzheimer’s disease, suggesting FTL1 could be a useful biomarker or therapeutic target.

“Our findings offer insight into one of the molecular drivers of age-related cognitive decline,” the researchers wrote. “While aging-related brain dysfunction is not necessarily linked to cell death, it is often tied to reduced synaptic activity and neural communication.”

The discovery adds to a growing body of research exploring how to maintain brain health and slow — or potentially reverse — cognitive decline. While further studies in humans are needed, researchers believe targeting FTL1 could pave the way for treatments addressing both natural aging and neurodegenerative disorders.