One protein keeps aging brain cells stable
The brain has a built-in mechanism to prevent nerve cells from becoming overactive. Researchers have now identified which protein plays a key role in that process, and what goes wrong when it is missing.
Sodium channels are proteins in the cell membrane of nerve cells that transmit electrical signals. When a nerve cell is active for a sustained period, these channels enter a dormant state, a process called slow inactivation. This protects the brain from overexcitation. But what exactly regulates this process was not well understood.
PRRT2 as a regulator of neural stability
Researchers identified the protein PRRT2 as a regulator of this process. PRRT2 causes sodium channels to enter the dormant state more quickly and remain there longer. This effect was found in both zebrafish and human cells, suggesting the mechanism has been evolutionarily conserved.
In mice lacking PRRT2 in the cerebral cortex, sodium channels responded more slowly to overactivation. As a result, the brain lost its resilience under stress, according to the researchers. The study was published in the journal eLife.
What does this mean for neurodegeneration and aging?
PRRT2 has long been known as a gene whose mutations cause epilepsy and movement disorders. What is new is that the protein also regulates the normal stability of the healthy brain, not just disease processes. That distinction matters.
As we age, the brain gradually loses its ability to dampen overactivation. If PRRT2 plays a role in that, it is a potential target for intervention. This is early mechanistic research, not a clinical application. But it establishes a link between sodium channel regulation and the resilience of the aging brain, a direction that warrants further investigation.
Search terms to explore further: sodium channel slow inactivation neurons, cortical hyperexcitability aging, PRRT2 epilepsy ion channel