Dr. Steven DeKosky is professor of Alzheimer’s research at the University of Florida College of Medicine and Deputy Director of the McKnight Brain Institute at that institution. He also is a professor of neurology and neuroscience there. Previously, he served as vice president and dean of the University of Virginia School of Medicine and was chairperson of the department of neurology at the University of Pittsburgh. Part 2 For the short-term, with mild to moderate traumatic injury you can have altered synaptic structure and function. For the longer term, chronic inflammation and chronic oxidative stress can lead to subsequent degeneration and also some chronic microglial activation, which may turn on mechanisms that you do not necessarily want, including cleaning up partially injured neurons that may recover. Especially in patients who get the disease in an older age, there is other pathology in the CTE. There are nerve fibrillary tangle and Lewy body.  Amyloid beta can be elevated in both white matter and grey matter and might add to the cascade that is thought amyloid leads to, which leads to degeneration especially Alzheimer’s disease, but cannot prove it. Participants in contact sports all are at significant risk. APOE 4 increases the risk of Alzheimer’s disease and the risk of tau deposition. Currently, when patients arrive for rehabilitation, they are going to have things a lot better described than was the case previously.  We can look at disruption of structures, see hemorrhage and inflammation. We know that CTE is not a new disease, but we do see the pathology in other contact sports and we do not view it in autopsy series unless the individual had a history or repetitive head injury. A Question & Answer period followed.