traumatic brain injury and Alzheimer's disease

Traumatic Brain Injury and ADRC Research

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Under the leadership of UW ADRC Associate Director, Elaine Peskind, MD, we have initiated major research efforts funded by the Department of Veterans Affairs to unravel the relationships between traumatic brain injury (TBI) and Alzheimer's disease and related dementing disorders. Our Center is using multiple advanced brain imaging techniques, measurement of biomarkers in spinal fluid, and careful neuropsychological testing to determine these relationships in veterans who have returned from Iraq and Afghanistan, athletes who have experienced sports-related concussions, and others in the community. These studies have great promise to develop new targets for the prevention and treatment of Alzheimer's disease and related dementing disorders.

 

The TBI and Alzheimer's Connection

Traumatic brain injury remains the only well-established environmental risk factor for Alzheimer's disease. Moderate to severe traumatic brain injury even early in life clearly increase the risk for Alzheimer's and even a single concussion (brain trauma severe enough to cause loss of consciousness) may increase the risk for Alzheimer's disease. Important links are emerging in clinical and laboratory studies of the immediate, as well as long-term, brain responses to traumatic brain injury. These responses involve the abnormal presence of brain chemicals that are central to Alzheimer's, beta amyloid and tau. Immediately after traumatic injury, the brain produces large amounts of beta amyloid, the very same protein that appears toxic to brain neurons when it is present in excessive amounts over many years in Alzheimer's. In Alzheimer's, beta amyloid gradually concentrates into the amyloid plaques that are a central diagnostic feature of the disease at an autopsy examination of the brain. Intriguingly, this deposit of beta amyloid into plaques does not occur following traumatic brain injury. If we can figure out what prevents plaque formation despite large beta amyloid release in response to brain trauma, we may be able to prevent the formation of toxic beta amyloid deposits in people with Alzheimer's disease.

The long term brain response to traumatic injury provides another link to Alzheimer's. Abnormal tau in the form of neurofibrillary tangles in damaged brain neurons in Alzheimer's is also seen as a long term consequence of traumatic brain injury. First described in boxers who became "punch drunk" in midlife, these tau neurofibrillary tangles are increasingly being found in the brains of football players and other athletes who have suffered repeated concussions from head trauma. These traumatic brain lesions and the cognitive loss they cause are properly called "chronic traumatic encephalopathy" or "CTE". This disorder is of increasing concern to our military because of the very common brain traumas suffered by our service members in combat in Iraq and Afghanistan.