Chrdl1 Loss of Function Mutation Increases Synaptic Plasticity in Mice

Researchers here suggest that the protein chrdl1 plays an important role in the regulation of synaptic plasticity, the ability of the brain to generate new connections between neurons. Synaptic plasticity declines with age, and is important in cognitive function. There is thus considerable interest in ways to enhance plasticity, not just to turn back this aspect of aging, but also potentially as a form of enhancement therapy to improve memory or other aspects of the mind.

Researchers have shown that astrocytes - long-overlooked supportive cells in the brain - help to enable the brain's plasticity, a new role for astrocytes that was not previously known. The findings could point to ways to restore connections that have been lost due to aging or trauma. "To investigate this role, we used a lot of techniques in the lab to identify a signal made by astrocytes that's very important for brain maturation."

The signal turned out to be a protein astrocytes secrete called Chrdl1, which increases the number and maturity of connections between nerve cells, enabling the stabilization of neural connections and circuits once they finish developing. To further understand the role of Chrdl1, the team developed mouse models with the gene disabled by introduced mutations. These mice had a level of plasticity in their brains that was much higher than normal. Adult mice with the Chrdl1 mutation had brain plasticity that looked very much like that of young mice, whose brains are st...

Source: Fight Aging! - October 22, 2018 Category: Research Authors: Reason Tags: Daily News Source Type: blogs