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 to stop or reverse disease progression.

Growing evidence suggests that glial-neuronal interactions and mitochondrial signaling are involved in aging-related disorders, including AD and FTD. Greater insight into glial and mitochondrial biology may hold the keys to prevention and effective treatments for these disorders and other conditions that have common underlying mechanisms.

We are investigating whether and how genes, proteins, and other factors linked to these disorders impair glial cells and mitochondria and disrupt glial-neuronal interactions that are critical for normal brain activities and resilience to disease.

Astrocytic-Neuronal Interactions and Glial Pathobiology

Glial cells, including astrocytes, are abundant non-neuronal cells that enable and regulate brain function. We are exploring the molecular mechanisms by which astrocytes affect brain function and influence impairments in neurodegenerative disease. Our main questions include:

1. How do astrocytes modulate neurons and engage in intercellular communication?

2. How do astrocytes affect behavioral and neurocognitive functions?

3. What are the roles of astrocytes in aging and neurodegenerative diseases?

4. Does therapeutic targeting of aberrant glial signaling and glial-neuronal interactions offer a promising treatment strategy for neurological disorders? 

Mitochondrial Reactive Oxygen Species

We are also interested in mitochondrial production of reactive oxygen species (also known as free radicals) and their contributions to glial signaling, neuronal functions, and neurodegeneration. We are pursuing the following questions in this area:

1. How are reactive oxygen species produced in neural cells in health and disease?

2. How do reactive oxygen species affect signaling and downstream functions in neurons and glia?

3. What are their roles in aging and neurodegenerative disease?

4. Can blockade of their production reduce or prevent neurological disorders?