Our lab is studying α synuclein as well as parkin, another gene associated with the juvenile form of Parkinson's disease. We are working to unveil the mechanisms by which mutations in the two genescan lead to familial Parkinson's disease, and how these mechanisms relate to the normal cellular roles of these genes. We employ molecular biological, cellular, and mouse genetic techniques to identify the proteins that interact with these genes.

Selected Recent Publications:

• Abeliovich, A., Schmitz, Y., Farinas, I., Choi-Lundberg, D., Ho, W.H., Castillo, P.E., Shinsky, N., Verdugo, J.M., Armanini, M., Ryan, A., Hynes, M., Phillips, H., Sulzer, D., and Rosenthal, A. (2000). "Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system." Neuron 25: 239-52.
• Staropoli, J.F., McDermott, C., Martinat, C., Schulman, B., Demireva, E., and Abeliovich, A. (2003). "Parkin is a component of an SCF-like ubiquitin ligase complex and protects postmitotic neurons from kainate excitotoxicity." Neuron 37: 735-49.