Axonal degeneration and glial/axonal interactions in disease


Our lab studies the interactions between glia and axons that are required for proper nerve function. Axonal dysfunction and degeneration are early and causative events in nervous system disorders ranging from traumatic injury to inherited and acquired peripheral neuropathies to neurodegenerative diseases like Alzheimer’s disease and Multiple Sclerosis. Axonal degeneration is an active, evolutionarily conserved, self-destructive process analogous to apoptosis but whose molecular underpinnings are largely obscure.  We have focused on dissecting the protection of damaged axons that is afforded by overexpression of Nmnat, an enzyme best known for its role in NAD biosynthesis. Peripheral axons are surrounded by Schwann cells, which provide them with important support, as evidenced by the axonal loss triggered by deficits in these glial cells.  Most recently, we have explored the impact of mitochondrial dysfunction as well as the roles of metabolic regulators such as AMPK, sirtuins and enzymes involved in NAD biosynthesis in modulating nervous system function. Our studies use in vitro and in vivo assays along with high throughput robotic, genomic and imaging methodologies. Our overall goal is to define the molecular pathways that regulate axonal stability and utilize this knowledge to develop methods to prevent axonal degeneration and treat disease.

Our lab is composed of a highly skilled team of research professors, postdocs and graduate students from around the world. We also have a knowledgeable and experienced research staff that provides the technical support required to speed discovery. We promote a lab environment that is collaborative and friendly where individual achievement and shared success are valued equally.  Postdoctoral fellows are encouraged to develop their own projects that they can pursue independently when they establish their own laboratories. Students find the environment supportive and the focus on translational neuroscience both exciting and rewarding.