summary: Aging shows memory by increasing the levels of FTL1 protein in the hippocampus, as it shows new research. In mice, the excess FTL1 caused the growth of normal neurons and led to a decrease in memory, while reducing FTL1 unlike these disabilities.
Old mice with the pent -up ftl1 have regained young nerve connections and better performance of memory tasks. The results indicate that the FTL1 ban may open a path towards treatments that restore the cognitive function in the brains of aging.
Main facts
- Discover ftl1: Top levels of FTL1 in ancient minds weaken nerve and memory connections.
- The effect of reflection: Reducing the delivery of youthful brain and memory in old mice.
- Therapeutic capabilities: The targeting of FTL1 may enable treatments that reflect age -related decrease.
source: Ucsf
Aging is especially harsh on the hippocampus, the brain area responsible for learning and memory.
Now, researchers at the University of California in San Francisco identified a protein located in the center of this decline.
Look at how genes and proteins change in the hippocampus over time in mice and found only one protein that differs between old and young animals. It is called FTL1. Old mice had more FTL1, as well as a lower connection between the brain cells in the hippocampus and the decreasing cognitive capabilities.
When artificial researchers increased FTL1 levels in small mice, their brains and behavior began to resemble those in ancient mice. In experiments in Petri dishes, nerve cells designed to make a lot of ftl1 nerve wires with a single weapon, or neurons, instead of the branched neurons created by normal cells.
But when scientists reduce the amount of FTL1 in the hippocampus of the old mice, they recovered their youth. They had more links between neurons, and mice were better in memory tests.
“The Paper, who appears at the UCSF Bakar Aging Confer The aging of nature On August 19. “It is much more than just delay or prevent symptoms.”
In ancient mice, FTL1 also slows the metabolism in hippocampus. But treating cells with a compound stimulates metabolism prevented these effects. Villeda is optimistic that the work can lead to treatments that prevent the effects of FTL1 in the brain.
“We see more opportunities to reduce the worst consequences of aging,” he said. “It is a superior time to work on aging biology.”
Authors: Others are UCSF are Laura Remissal, PhD, Juliana Sucharov Kososa, Carishma GB Prat, PhD, Gregor Perry, Ph.D. Philip, PhD, Mason Van, Turan Agayev, PhD, Charles Way White, C. Maynard, PHD, Alma L. Burlingame, PhD. All authors see the paper.
Finance: This work was partially funded by the Simons Foundation, the Bakar Family Foundation, the National Science Corporation, the Helbum Foundation, the Bakar Armakha Institute, Mark and Lin Benioff, and the National Institutes of Health (AG081038, AG067740, AG062357, P3063720). For all financing see the paper.
About news of heredity, aging and memory research
author: Levi Goldi
source: Ucsf
communication: Jadi – UCSF
image: The image is attributed to news of neuroscience
The original search: Open access.
“Targeting the FTL1 iron -related protein in the brain of ancient mice improves the cognitive weakness associated with ageWritten by Laura Remissal and others. The aging of nature
a summary
Targeting the FTL1 iron -related protein in the brain of ancient mice improves the cognitive weakness associated with age
It is necessary to understand the cellular and molecular motives of age -related cognitive decline to determine the goals to restore awareness of aging.
Here we define the Veritin 1 (FTL1) series, which is a protein associated with iron, as a pro -aging neurological factor that weakens perception.
Using the hematomatic and massive measurement approaches, we discover an increase in the nervous FTL1 in the hippocampus of the elderly mice, whose levels are associated with cognitive decline.
Simulation of age associated with FTL1 neurons in small mice change the cases of core iron oxidation and enhance the interlocking and cognitive features of the hippo.
The targeting of FTL1 neurons in the hippocampus of elderly mice improves interlocking molecular changes and cognitive weakness.
Using the neuronal DNA sequence, we discover changes in metabolism, such as ATP synthesis, and enhance these metabolic functions through NADH supplements reduce the effects of aging from the nerve FTL1 on perception.
Your data FTL1 determines neurons as a major molecular medium for cognitive regeneration.
2025-08-20 17:46:00
