Our research is directed toward the understanding of the molecular mechanisms underlying HD. Previous work by us and collaborators has shown that one of the early dysfunctions triggered by mutant huntingtin is aberrant metabolism of specific lipids such as cholesterol and gangliosides. These lipids are important components of membrane microdomains known as "lipid rafts" that serve as hubs for cell signaling, and that are crucial to the function of the nervous system, to synaptic transmission and cell-cell communication. Projects in our laboratory are mainly focused on understanding the effects of brain lipid dysregulation on function and survival of HD neurons, and on identifying the underlying mechanisms and potential therapeutic treatments.
For our research we use transgenic animal and cell models of HD, as well as cell lines derived from HD patients. Our experimental approach is multidisciplinary, involving biochemical, molecular and cell biology techniques.