Huntington’s Disease (HD) is a fatal neurodegenerative disease that results in neurological and motor impairments that worsen after onset over a period of 10-25 years. HD is caused by an expanded polyQ gene characterized by increased CAG repeats. Specifically, HD causes degeneration of medium spiny neurons, located in the striatum. We studied the pathogenesis in a novel HD murine model containing approximately 200 CAG repeats inserted in the mouse homolog of the human HD gene, Hdh. This HdhQ200/200 mouse more closely mimics the symptomology of HD than the current mouse models, which do not completely imitate the HD phenotype seen in humans. The HdhQ200/200 model also allows for improved analysis of gene involvement in HD development. Previous models show decreases in neuronal protein expression responsible for functions including glutamate transport, cAMP regulation, initiation of glycolysis, and other similarly ubiquitous functions such as anchoring synaptic proteins. In addition, the CB1R gene, which is a significantly known early marker for the onset of human HD pathology, also shows decreased expression in previous mouse models. Decreased expression of these proteins causes widespread neuronal dysfunction, characteristic of HD symptomology. Here, we examine neuronal protein expression in this novel HdhQ200/200 model using western blotting technique to see if these proteins are similarly down regulated, indicating that this model could be an alternate method of studying HD in mice. This would provide substantiating evidence that the HdhQ200/200 mouse is an appropriate model for HD, which would allow for more accurate research into HD pathogenesis and symptomology that could help current HD patients