Gene Linked to Huntington's Disease Important for Normal Memory Development

More than 20 years have passed since scientists first stumbled onto the gene responsible for Huntington's, a progressive neurological condition that wreaks havoc on the body, resulting in involuntary movements, emotional disturbances and cognitive impairment. Relatively little has been known about the gene's role in normal brain function, since. 

Now, a recent study from The Scripps Research Institute's (TSRI's) Florida campus and Columbia University found that it plays a critical role in long-term memory.

"We found that huntingtin expression levels are necessary for what is known as long-term synaptic plasticity-the ability of the synapses to grow and change-which is critical to the formation of long-term memory," said TSRI Assistant Professor Sathyanarayanan V. Puthanveettil, who led the study with Nobel laureate Eric Kandel of Columbia University, in a news release.

For the study, researchers identified an equivalent of the human huntingtin protein in the marine snail Aplysia. This widely used animal model for various genetic studies often works as a human counterpart, with proteins that are widely expressed in neurons throughout the central nervous system.

Findings revealed RNA expression of huntingtin were increased by serotonin, a neurotransmitter that's relaeased during learning in Aplysia. After getting rid of the huntingtin protein, however, the neurons failed to function properly.

"During the learning, production of the huntingtin mRNAs is increased both in pre- and post-synaptic neurons-that is a new finding," Puthanveettil added. "And if you block production of the protein either in pre- or post-synaptic neuron, you block formation of memory."

Researchers believe that these findings could assist with the development of future treatments for the disorder. However, they also caution that the results go against a therapeutic approach that eliminates the protein, altogether.

More information regarding the findings can be seen via the journal PLOS ONE.