Research Interests

One of our research interests is to elucidate signal transduction mechanisms that regulate the fate of neural stem cells, i.e. what makes a neural stem cell proliferate and differentiate into neurons or glia in the mammalian brain. We are interested in neural stem cell regulation both during development and in adult neurogenesis. Specifically, recent studies in our lab suggest a novel role for the extracellular-signal-regulated kinase 5 (ERK5) MAP kinase in regulating the fate choice of cortical stem cells during development. The elucidation of molecular mechanisms that regulate neural progenitor cell proliferation and differentiation is important for an understanding of neural developmental and neurodegenerative diseases. Furthermore, stem cell-based cell replacement therapy offers enormous potential for the treatment of a variety of developmental, psychiatric, neurodegenerative and aging related diseases for which there are currently no cures. Moreover, environmental toxicants may cause developmental neurotoxicity by perturbing these signaling mechanisms that regulate neurogenesis.
II. MECHANISMS FOR REGULATION OF NEURONAL APOPTOSIS
Our laboratory is also
interested in molecular mechanisms and signal transduction pathways that
regulate neuronal survival and cell death. It has become increasingly evident
that many environmental toxicants might contribute to the development of
neurodegenerative disorders including Parkinson's disease, Huntington's disease,
and Alzheimer's disease. Our recent effort has focused on elucidating signaling
mechanisms that regulate dopaminergic neuron cell death in relation to
Parkinson’s disease using exposure to several pesticides as model systems. It is
our hope that these mechanistic studies may ultimately lead to the development
of pharmacological interventions and clinical strategies for treatment of
Parkinson’s disease. These studies may also provide insights concerning the
relationships between environmental toxicants and the etiology of
neurodegenerative disorders.
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