In Huntington’s disease, the first evidence of damage in the brain occurs in the part of the brain called the striatum; D1 and D2 neurons constitute 90% of neurons in the striatum.

It was previously thought that dopamine neurons, called D2 neurons, were responsible for the devastating symptoms seen in Huntington’s disease but researchers at Melbourne’s Howard Florey Institute have proven that loss of D1 neurons causes many of the disabling symptoms of the diseases.

Their discovery could be said to have opened up new treatment possibilities for the Huntington’s.

Research leader John Drago, said now that the importance of D1 neurons in HD had been established, they could work towards therapies that focused on both D1 and D2 neurons.

“Currently there is no effective treatment for Huntington’s disease and patients suffer from debilitating movement, memory, and psychiatric problems,” he said.

Drago’s discovery was made after he genetically engineered a mouse with damaged D1 neurons alone but which still developed the Huntington’s.

While a mouse model that carries the human Huntington's disease gene already exists, Drago’s mouse model is the first in the world to accurately mimic the death of the D1 neurons in the striatum.

“Despite the widespread death of D1 neurons, the mouse was healthy, apart from having HD symptoms,” he said.