Scientists at the University of California San Francisco (UCSF) may have discovered a cause of aging in the brain, identifying a protein called ferritin light chain 1 (FTL1) as a key factor in age-related cognitive decline. Published in the journal *Nature Aging*, the study reveals that FTL1, an iron-associated protein, acts as a ‘pro-aging neuronal factor’ that impairs cognition. Researchers compared gene and protein expression in the hippocampus, the brain’s memory center, in young and old mice, finding that aged mice had higher levels of FTL1, along with fewer nerve connections and diminished cognitive abilities. When FTL1 was artificially increased in young mice, their brains and behaviors mirrored those of older mice, while reducing FTL1 in aged mice led to improved memory and restored youthful brain function. The study suggests that targeting FTL1 could open new avenues for reversing age-related cognitive decline.
Dr. Saul Villeda, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, emphasized that these findings represent a ‘reversal of impairment,’ stating that the results go beyond merely delaying symptoms. ‘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 aging,’ Villeda said in a press release. The study also found that treating cells with a metabolism-stimulating compound prevented the negative effects of elevated FTL1. Dr. Paul Saphier, a neurosurgeon and founder of Coaxial Neurosurgical Specialists, called the findings ‘really interesting,’ noting that the accumulation of certain proteins in the brain is linked to neurodegenerative disorders like Alzheimer’s. Saphier suggested that if FTL1 buildup can be slowed or reversed in the hippocampus—the brain’s memory center—cognitive decline may be mitigated. Previous research has shown that modulating sugar and protein intake can influence the rate of aging, further supporting the potential for lifestyle and therapeutic interventions.
The University of California San Francisco received support for the study from the National Science Foundation, the Bakar Aging Research Institute, and the National Institute on Aging. These findings align with a growing trend in aging research, where scientists are increasingly focusing on the biological mechanisms that drive cognitive decline and exploring potential therapeutic strategies. As the global population ages, the implications of this research could extend beyond mice, offering hope for developing interventions that target age-related neurodegenerative conditions. Researchers are now working to translate these findings into human studies, potentially paving the way for new treatments that could improve the quality of life for older adults.