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Posted On: 08/21/2025 7:02:28 AM
Post# of 156193
Scientists have found a protein that, when reduced, can slow aging in the brain. By reducing this protein, they can restore cognition in old mice. Some of the factors shown to increase this protein are inflammatory cytokines, such as: IL-1 and TNFa. These are inflammatory cytokines that are reduced by blocking the CCR5 receptor. It appears that science is finding more and more mechanisms showing inflammation might play a larger role in cognitive decline. Interesting reading here. It looks like another mechanism of action of Leronlimab, for treating cognitive decline, is described.
"When the researchers artificially increased FTL1 levels in young mice, their brains and behavior began to resemble that of old mice.
In experiments in petri dishes, nerve cells engineered to make lots of FTL1 grew simple, one-armed neurites -- rather than the branching neurites that normal cells create.
But once the scientists reduced the amount of FTL1 in the hippocampus of the old mice, they regained their youth. They had more connections between nerve cells, and the mice did better on memory tests.
"It is truly a reversal of impairments," said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, which appears in Nature Aging on Aug. 19. "It's much more than merely delaying or preventing symptoms."
In old mice, FTL1 also slowed down metabolism in the cells of the hippocampus. But treating the cells with a compound that stimulates metabolism prevented these effects."
Scientists just found a protein that reverses brain aging | ScienceDaily https://www.sciencedaily.com/releases/2025/08...000808.htm
"Although the IRP/IRE regulation of ferritin synthesis is the predominant pathway that allows an adaptive increase, several other mechanisms, such as IL-1, TNFα, hypoxia, and oxidative stress have also been observed to regulate ferritin expression (23, 169, 170, 173, 184). It is likely that a combination of these pathways allow an efficient increase in ferritin when required."
Iron homeostasis in the liver - PMC https://share.google/kon92Smuo6eqt8a7u
"When the researchers artificially increased FTL1 levels in young mice, their brains and behavior began to resemble that of old mice.
In experiments in petri dishes, nerve cells engineered to make lots of FTL1 grew simple, one-armed neurites -- rather than the branching neurites that normal cells create.
But once the scientists reduced the amount of FTL1 in the hippocampus of the old mice, they regained their youth. They had more connections between nerve cells, and the mice did better on memory tests.
"It is truly a reversal of impairments," said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, which appears in Nature Aging on Aug. 19. "It's much more than merely delaying or preventing symptoms."
In old mice, FTL1 also slowed down metabolism in the cells of the hippocampus. But treating the cells with a compound that stimulates metabolism prevented these effects."
Scientists just found a protein that reverses brain aging | ScienceDaily https://www.sciencedaily.com/releases/2025/08...000808.htm
"Although the IRP/IRE regulation of ferritin synthesis is the predominant pathway that allows an adaptive increase, several other mechanisms, such as IL-1, TNFα, hypoxia, and oxidative stress have also been observed to regulate ferritin expression (23, 169, 170, 173, 184). It is likely that a combination of these pathways allow an efficient increase in ferritin when required."
Iron homeostasis in the liver - PMC https://share.google/kon92Smuo6eqt8a7u
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