While further work still needs to be done to determine how the genetic mutation causes the excessive number and activity of NMDA receptors to localize outside the synapses, the researchers did find a way to mitigate damage and slow disease progression at early stages of the disease-using Memantine, a drug currently used to treat Alzheimer's disease.

"Memantine in low dose works by preferentially blocking the activity of NMDA receptors outside the synapse," says Dr. Michael Hayden, director of the Centre for Molecular Medicine and Therapeutics, professor in the UBC Department of Medical Genetics, and co-author on the study.

"It was previously shown to reverse deficits and damage in late stages of animal models of Huntington's disease, but we found it could improve learning and cell survival signaling even at early stages of the disease," says Hayden. "A small human clinical trial of Memantine for Huntington's disease has also recently shown positive effects. Larger, international clinical trials are now being planned."

"Memantine's beneficial effects appear to be dose-specific," Raymond adds. "Before it can be prescribed to treat Huntington's disease, we need to know how to determine appropriate dosing and whether it interferes with other essential cellular and brain functions."

Source: University of British Columbia