The goal of this project is to uncover molecular mechanisms underlying Huntington's disease. We are using tissue culture and animal models of this disease, and are pursuing the hypothesis that abnormalities in cellular responses to stress are critical in the disease process. The student role will be to conduct basic lab research as part of this project.
Brain injury in premature infants remains a very significant medical problem even as great strides have been made in helping these infants survive following early birth. We are trying to understand the special vulnerability of the premature brain to a variety of insults. Using tissue culture and whole animal models, our goal is to characterize mechanisms of injury and death in the developing CNS to provide the basis for developing effective prevention and treatment. The student will perform bench research using tissue culture and animal models of neonatal brain injury. The focus is on understanding the mechanisms underlying ischemic injury to oligodendrocytes and white matter in the developing brain at a cellular and molecular level.
We are interested in how glutamate concentration is controlled in and around excitatory synapses. Abnormalities in excitatory transmission have been found to be important in the pathogenesis of chronic neurodegenerative diseases (CNDs), in particular, Alzheimer's disease and Huntington's disease. Glutamate homeostasis is largely controlled by glutamate transporters, and the most important of these is GLT-1, which is expressed in both neurons and astrocytes. We have made a conditional GLT-1 knockout which permits the selective knock out of GLT-1 in the different cell types and regions in which it is expressed. Using this approach we are probing the role of GLT-1 expressed in axon terminals. The student will perform bench research and in vivo studies to understand how abnormalities in glutamate homeostasis in axon terminals may contribute to the pathogenesis of CNDs and mental illness.