Restoring a brain protein improved memory in aged mice
In an experiment in aged mice, re-expressing the protein increased the density of dendritic spines, small signal-receiving structures on neurons, and improved memory performance.
Limit: The report gives no duration for the memory improvement after TAK1 restoration
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in mice reported in a preprint, researchers examined transforming growth factor beta-activated kinase 1, an enzyme called TAK1. They conditionally reduced TAK1 in forebrain excitatory neurons, cells that transmit stimulating signals. This reduction impaired short- and long-term memory in the animals. In the hippocampus, a brain region that processes memory, the reduction weakened long-term potentiation, a persistent strengthening of cellular connections that supports learning. TAK1 deficiency also reduced the density of dendritic spines, small structures that receive signals, and suppressed excitatory signaling between neurons.
The researchers observed that synaptic TAK1 levels were reduced in the aged hippocampus. Re-expressing neuronal TAK1 in aged mice increased dendritic spine density. It also enhanced hippocampal synaptic plasticity, the capacity of connections to alter their strength, and improved memory performance.
Why it matters
The findings suggest that reduced TAK1 signaling may contribute to the hippocampus’s vulnerability during aging.
Caveats
The findings come from laboratory experiments in mice, so the signaling mechanism may not operate the same way in people. The work is also a preprint that has not yet undergone peer review.
The paper
bioRxiv, Oct 26, 2026, Open access, CC BY-NC-ND, Preprint, not peer-reviewed
