In Huntington's disease, neurons become more excitable and die. Researchers have now found a faulty ion channel in astrocytes, another type of brain cell, that could be contributing to this.
Baljit Khakh and Michael Sofroniew at the University of California, Los Angeles, and their colleagues studied two mouse models of Huntington's disease, and show that channels that allow potassium ions to cross the cell membrane were dysfunctional in astrocytes containing the Huntington's disease proteins. This caused potassium levels outside the cells to rise, making the membranes of nearby neurons more excitable.
The authors reversed these defects by replacing the faulty channels with functional ones. In one of the mouse models, channel replacement allowed the animals to walk more normally and live longer than mice with defective channels.