It is estimated that 1.7 million Americans will have a traumatic brain injury (TBI) each year. 75% of those TBIs are classified as a mild traumatic brain injury: also known as a concussion. It is widely assumed that the effects of a concussion, such as dizziness and headaches, are temporary. Evidence suggests that this is not the case and even a concussion can result in progressive brain atrophy. All blows to the head do not lead to neurodegeneration; however, they do increase the likelihood that someone may develop dementia in their lifetime.

My research is focused on understanding neuron-glia interactions that underlie complex diseases of the brain. We are particularly interested in how neuron-glia interactions are altered after a concussion, and how those alterations could increase the chance that someone may develop dementia. Glia are exquisitely sensitive to pathological changes in the brain. There are many supportive interactions of glia that maintain healthy CNS function. When glia become reactive, the supportive homeostatic functions can be lost in favor of reactive functions. Keeping the balance between supportive roles and reactive functions requires precise control over the temporal development of various glial responses after injury or in disease. Either abnormal glial responses or abnormal timing of glial responses can have a major impact on whether the outcome leads to clearance/resolution and maintenance of normal CNS function, or conversion to disease pathology. The overall goal of my research is to provide fundamental insights into how particular glia responses modify disease outcome and find targets amenable to selective therapeutic modulation of those specific functions.