Falling nuclear protein levels impair nerve signaling in mice
In male mice, boosting a nuclear protein at 12 months prevented age-related changes in nerve signaling and brain function assessed at 20 months.
Limit: Live-animal analyses included only male mice
Stake: Kawano Masanori Memorial Public Interest funded the study. Novartis funded the study.
Edited by Boris Djordjevic · AgingResearch.News
Experiments in male mice tested how declining levels of the LINC complex, a group of proteins on the membrane around the cell nucleus, affected nerve cells. Levels fell across several brain regions as mice aged. The axon initial segment—the part of a nerve cell where electrical signals begin—also shortened.
Researchers used a virus to increase production of Sun1, one of these nuclear proteins, in mice at 12 months and examined them at 20 months. Maintaining Sun1 prevented age-related shortening of this segment, impaired electrical signaling and changes in brain function. It also shifted DNA organization and gene activity toward patterns in young neurons. In a separate experiment, inhibiting the complex in young mice shortened the segment, reduced nerve cells’ ability to fire electrical signals and impaired brain function.
Why it matters
Brain function deteriorates with age, but its molecular drivers remain unclear. This work addresses how changes around the cell nucleus contribute to that decline.
Caveats
These animal experiments did not test whether the approach preserves brain function in people. All live-animal analyses used male mice.
- SUN1
- Chromatin and 3D genome organization
- Nuclear envelope
- Axon initial segment length
- LINC complex expression
- Mice
The paper
Shimane University
EMBO Reports, May 22, 2026, Open access
doi.org/10.1038/s44319-026-00786-5PubMed 42174181
Corrected, Jul 29, 2026
