Astrocytic and Microglial Receptor Signaling
Glia, including astrocytes and microglia, are abundant non-neuronal cells of the brain. We are exploring the signaling mechanisms by which astrocytes and microglia regulate brain function and affect neurological disorders. We examine how these cells are affected in disease and can contribute to cognitive dysfunction and neurodegeneration. Our main questions include:
1. How does glial receptor signaling modulate neural cell function and intercellular communication?
2. How does glial signaling affect neural network activity, cognitive function and behavior?
3. What are the roles of glial signaling in aging and neurodegenerative diseases, especially frontotemporal dementia and Alzheimer's disease?
4. Does therapeutic targeting of aberrant glial signaling offer a promising treatment strategy for neurological disorders?
Frontotemporal Dementia and Alzheimer's Disease
FTD and AD are devastating neurodegenerative disorders that cause progressive brain damage, impairments in cognitive function and abnormalities in behavior. The underlying causes of FTD and AD are not clear and no effective treatments are available.
New research suggests that glial cells may be involved in AD and FTD pathogenesis. Greater insight into glial cells may hold the keys to prevention and effective treatments for these disorders and other conditions that have common mechanisms.
We are examining whether genes and proteins linked to these disorders impair the functions of glial cells and disrupt glial-neuronal interactions that are critical for normal brain function and resilience to disease.
Mitochondrial Reactive Oxygen Species
We are also interested in mitochondrial production of reactive oxygen species and their contribution to glial signaling, neuronal function and neurodegeneration. We are pursuing the following questions:
1. How are reactive oxygen species produced in neural cells in health and disease?
2. How do they affect cell signaling and downstream functions?
3. What are their roles in aging and neurodegenerative diseases?
4. Can blockade of their production reduce or prevent neurological disorders?