A new study has revealed that a protein linked to declining brain performance may hold the key to reversing memory loss and preventing diseases such as Alzheimer’s.
اضافة اعلان
Increasing research shows that aging particularly affects the hippocampus, the brain region responsible for learning and memory. Aging is the dominant factor in neurodegenerative disorders such as Parkinson’s and Alzheimer’s.
The study, published in Nature Aging, concluded that the FTL1 protein is the main driver of this decline.
Researchers found that older mice have higher levels of FTL1, with fewer connections between brain cells in the hippocampus and reduced cognitive abilities compared to younger mice.
When researchers artificially increased FTL1 levels in young mice, their brains and behavior resembled those of older mice. Lab-grown neurons engineered to produce high levels of FTL1 also developed fewer branches.
The study noted: “We identified the FTL1 chain, an iron-related protein, as a neuro-aging factor that impairs cognition. We observed increased neural FTL1 in the hippocampi of aged mice, and its levels correlated with cognitive decline.”
However, when FTL1 levels were reduced in the hippocampi of older mice, their neural vitality was restored. These mice showed more connections between neurons and performed better in memory tests.
Researchers also observed that FTL1 slows metabolism in hippocampal cells, but treating these cells with the metabolism-boosting enzyme NADH prevented these effects.
They wrote: “Our data indicate that neural FTL1 is a key molecular mediator for reversing cognitive decline. This raises the exciting possibility that targeting neural FTL1 in aging could extend benefits beyond cognitive aging to neurodegenerative diseases in older adults.”
The study noted that enhancing metabolic function with NADH supplements alleviated the effects of aging on cognition. Researchers hope that therapies designed to counteract FTL1 effects in the brain will yield positive results for patients with dementia.
—Independent
