Recent research has shown a relationship between traumatic brain injury and Alzheimer's disease. Autopsy studies of people who had traumatic brain injury have revealed Alzheimer's-like plaques and tangles. It is also known that the APOE genotype is associated with both an increased risk of Alzheimer's disease and an increased risk of neural degeneration after brain injury.
Researchers recently discovered another potential connection. Amyloid beta, a protein that has normal functions within the body, is related to Alzheimer's disease when too much accumulates. Microglia are a type of brain cell that is primarily responsible for an immune response. Microglia are also important for recruiting and activating amyloid beta.
In response to a primary brain injury, the brain reacts with an immune response (a secondary injury), led by the microglia. The increase in microglia after a brain injury may result in an increased activation of the amyloid beta that will later become a risk factor for Alzheimer's disease. Much research has focused on the reduction of this secondary injury. Reducing the immune response may help prevent the increased risk for Alzheimer's-like degeneration after traumatic brain injury.
Mannix RC & Whalen MJ. Traumatic brain injury, microglia, and beta amyloid. International Journal of Alzheimer's Disease. (June 2012).