As people age, they often find that their memories fade and learning new things becomes difficult. Researchers in the United States have found clues that cause brain aging and even confirmed the possibility of reversing aging in animal experiments.
On the 19th, a research team from the University of California, San Francisco (UCSF) published findings in the international journal "Nature Aging" that a protein called "FTL1" related to iron may be the key to reversing memory decline due to aging.
The research team focused on analyzing the hippocampus, the area of the brain responsible for learning and memory. Comparing genetic and protein changes between young and old mice revealed significant differences in the protein FTL1. Older mice had higher levels of FTL1, and the consolidation between neurons in the hippocampus decreased, leading to a noticeable decline in cognitive abilities.
The researchers explained that an increase in FTL1 promotes the accumulation of iron oxide in hippocampal neurons. This can lead to oxidative stress, mitochondrial dysfunction, and ultimately neuronal damage, potentially causing neurodegenerative diseases like Alzheimer's.
The research team also conducted experiments to directly confirm the role of FTL1. When FTL1 was artificially increased in the brains of young mice, their brain activity and behavior quickly resembled those of older mice. Conversely, reducing FTL1 in the brains of older mice made the consolidation between neurons active again and resulted in memory test scores comparable to young mice.
Saul Villeda, the deputy director of the UCSF Buck Institute for Research on Aging, noted, "This is not just about slowing aging; it actually reverses damaged functions," adding that "it has truly reversed brain dysfunction."
Cellular experiments also showed intriguing results. Observing individual neurons in culture dishes revealed that cells with high levels of FTL1 had neurites that were supposed to branch out like tree branches extending in only one direction. This identified the cause of why neurons fail to function properly. However, when compounds that promote cellular metabolism were applied, this phenomenon was suppressed.
The researchers stated that this discovery could lead to the development of treatments for degenerative brain diseases like dementia. If a treatment that blocks the action of FTL1 in the brain is developed, it could not only slow down memory decline due to aging but also revive lost memory and learning capabilities.
Deputy director Villeda remarked, "This research may lead to the development of treatments that block the effects of FTL1 in the brain," adding that "now is a hopeful time for researching the biology of aging."
Recently, substances that can slow down or reverse cognitive decline due to aging have gained attention. A research team led by Bruce Yankner from Harvard Medical School noted in a paper published on the 6th in Nature that lithium levels in the brain are essential for maintaining cognitive function.
The research team provided animal experiment results indicating that a decrease in lithium in the brain promotes Alzheimer's, while conversely, supplementing lithium restores cognitive function. They also discovered that lithium in the brains of mice binds with amyloid plaques, which are identified as a cause of Alzheimer's, leading to decreased cognitive function.
References
Nature Aging (2025), DOI: https://doi.org/10.1038/s43587-025-00940-z
Nature (2025), DOI: https://doi.org/10.1038/s41586-025-09335-x