Our lab is working to better understand the mechanisms of cellular damage in traumatic brain injury and in Alzheimer’s disease. We are particularly focused on the ways trauma and neurodegeneration affect synapses, the gray matter nodes at which neurons communicate to form functional networks.
Traumatic brain injury is the major cause of neurological morbidity and mortality for individuals in the first half of life, and the best established environmental risk factor for the development of Alzheimer’s disease, the scourge of the second half of life. We recently developed a new method to quantify synapses called SEQUIN, and applied this technique to identify synaptic loss after TBI. We are now working to reveal the relationship between this process and dementing illnesses.