After UVA Health researchers made the shocking discovery that the brain and immune system are connected, they had to rewrite the textbooks. UVA Health's Center for Brain Immunology and Glia (BIG) remains at the forefront of neuroimmunology research.
A researcher at BIG, John Lukens, PhD, works to understand how the immune and nervous systems interact. The goal is improved understanding of complex neurological disorders like Alzheimer's, multiple sclerosis, and traumatic brain injury.
From there, Lukens hopes to identify new promising therapeutic targets for these conditions.
Watch Lukens describe his research.
What are you working on right now?
We are exploring how to harness the immune system to treat neurological diseases. In particular, our lab has been most recently engaged in studies to define how the major immune cell population of the brain, microglia, can be leveraged to limit neurological disease progression.
Microglia are specially equipped to safely dispose of neurotoxic agents that can cause neuronal cell death. Microglia can become dysfunctional with aging and in response to various environmental and genetic factors.
Our lab has been actively involved in efforts to uncover novel molecular players that can be therapeutically targeted to rejuvenate beneficial microglial responses as a strategy to prevent and/or reverse brain damage and dysfunction.
What are the most intriguing potential clinical applications of your work?
Our lab is especially interested in the potential of targeting microglia as a therapeutic option to treat neurodegenerative diseases. In our microglia studies, we have identified a number of novel molecules that can be targeted to protect against Alzheimer’s disease progression, which is the most common form of dementia.
Our recent work shows that inhibiting the phosphatase SHIP-1, which we have identified to be a molecular brake on beneficial microglial responses, is highly effective in limiting neurodegenerative disease pathogenesis in experimental models of Alzheimer’s disease.
We have also found that pharmacological activation of the molecules CLEC7A, SYK, and CARD9 can provide an effective strategy to rejuvenate neuroprotective microglial responses and curb neuropathology in experimental models of Alzheimer’s disease.