- Department of Pathology & Cell Biology
- Department of Neurology
- Associate Professor of Pathology and Cell Biology and Neurology (in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain)
We are studying the molecular bases of midbrain dopamine neuron development, function and survival. Midbrain dopamine neurons are thought to play key roles in learned and addictive behaviors, and degeneration of these neurons underlies Parkinson's disease.
A focus of the lab is to understand the mechanisms by which mutations in Parkinson's disease-related genes, such as a-synuclein and parkin, lead to midbrain dopamine neuron dysfunction and eventual demise. We are also particularly interested in the normal cellular roles of these genes. We use a combination of molecular biological, cellular, and mouse genetic approaches to this end.
In a second project, we are characterizing molecules that play a important roles in the specification and late development of dopamine neurons using an in vitro culture system. Embryonic stem cells have been shown to give rise to dopamine neurons in response to a set of extrinsic cues such as sonic hedgehog and FGF8. Furthermore, a few intrinsic cellular factors, such as nurr1, have been implicated in the generation of dopamine neurons. We are using molecular biological tools to investigate the mechanism by which such intrinsic signals determine midbrain dopamine neuron fate.
Education & Training
Primary Lab Locations
William Black Building
650 West 168th Street
12th Floor, Room 1208
New York, NY 10032
- (212) 305-1150
Staropoli, J. F., McDermott, C., Martinat, C., Schulman, B., Demireva,E, and Abeliovich, A. (2003). Parkin is a Component of an SCF-likeUbiquitin Ligase Complex and Protects Postmitotic Neurons from KainateExcitotoxicity. Neuron 37: 735-749.
Abeliovich, A., Schmitz, Y., Farinas, I., Choi-Lundberg, D., Ho, W.-H., Verdugo, J. M. G., Armanini, M., Ryan, A., Hynes, M., Phillips, H., Sulzer, D., and Rosenthal, A. (1999). Mice lacking a-synuclein display functional deficits in the nigrostriatal dopamine system. Neuron 25, 239-252.