Laboratory for Brain Injury and Dementia
Traumatic Brain Injury (TBI): an insult to the brain from an external force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions.
Chronic Traumatic Encephalopathy (CTE): a progressive degenerative disease of the brain found in athletes or persons with a history of repetitive concussions
The Laboratory for Brain Injury and Dementia (LBID) at Georgetown University uses in vivo brain trauma models to understand how traumatic brain injury (TBI) impacts normal brain function, and why it can result in the activation of pathways involved in chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson’s disease, and chronic traumatc Encephalopathy (CTE). Our overarching goal is to understand how and why neurodegenerative pathways are active after severe TBI or repeat mild TBI (mTBI), resulting in the development of dementias, such as Alzheimer's disease and chronic traumatic encephalopathy (CTE). CTE has been best reported in boxers, but has been found in the brains of NFL players, wrestlers, hockey players, abuse victims, and people who have suffered repeat concussions throughout their lives.
A major function of our lab is to design and characterize in vivo models of concussion. By definition a concussion, or mild traumatic brain injury (mTBI) is a temporary loss of brain function that is spontaneously recoverable. How then can a mTBI trigger a disease process in the brain? We have found that a mild head trauma, even in the absence of cell death or inflammation, can cause a spontaneously recoverable loss of synapses - the physical connection between neurons. Surprisingly, when the number of concussions are increased the brain adapts to the head trauma. These data are indicative of a rewiring of the synapse in response to increased mTBI exposure - however we do not yet understand the nature or long-term consequence of this rewiring. Importantly when the time period between mTBI is at least one week, this rewiring does not occur.
Another major area of interest is understanding how and why severe brain trauma causes the rapid production of amyloid-beta and hyper-phosphorylated tau - classic hallmarks of Alzheimer’s disease and CTE. Accumulation of amyloid-beta after TBI may impair functional recovery and exacerbate the severity of the injury. We have found that traumatic axonal injury causes the production of amyloid and p-tau, and that factors such as the APOE4 gene can interfere with the efficient clearance of amyloid from the brain.
Contusion, concussion and penetrative brain trauma models are the most commonly used models in the LBID, and the lab has the capability to perform surgery, behavioral and biochemical aspects of this research. We also take advantage of the outstanding core imaging facilities available at Georgetown University, including a small animal imaging laboratory with a 7Tesla magnetic resonance imager, confocal microscopy, stereology, fluorescent and standard microscopy.
From Washington, Villapol, & Burns. Exp Neurology (2016) 275:381- 388