American scientists have identified a protein, FTL1 (ferritin light chain 1), whose accumulation in the brain may accelerate age-related memory decline. Levels of FTL1 were found to be significantly higher in the hippocampus of older mice compared to younger ones. The more FTL1 present, the worse the animals performed on cognitive tests. This groundbreaking research was published in the journal Nature Aging.
When researchers artificially increased FTL1 levels in young mice, their cognitive abilities worsened, showing reduced synaptic plasticity, impaired neuronal function, and “aged-like” memory. Conversely, reducing FTL1 levels in older mice led to improved synaptic activity and a restoration of memory function.
Molecular analysis revealed that FTL1 impacts iron metabolism in neurons and disrupts energy production processes, primarily ATP synthesis. Researchers found that supplementing cells with additional coenzyme NADH could partially alleviate these metabolic and cognitive impairments.
The authors emphasize that their study is the first to identify FTL1 as a key factor in cognitive aging and a promising therapeutic target. If these findings are confirmed in human studies, it could pave the way for novel strategies to prevent age-related memory loss and dementia.
Previously, scientists at Harvard demonstrated that a specific form of lithium can not only slow down but also reverse brain damage associated with Alzheimer`s disease.
