One of the strongest risk factors for Alzheimer’s disease is traumatic injury to the brain. Mouse research now shows that injury leads to changes in two important proteins that help brain cells communicate. In addition, and possibly as a result, the level of an enzyme called BACE1 rises. With more BACE1 circulating in the brain, amyloid beta levels also soar.
Post-mortem examination of people with Alzheimer’s disease show that these chemical changes are also present in humans with the disease. The brains of people who did not have Alzheimer’s when they died do not show these alterations. The hope is that this research will help scientists find a way to control the BACE1 enzyme in people who have suffered traumatic brain injury. No one knows if regulating BACE1 might lead to a new and different approach to treating Alzheimer’s disease.
[Journal of Neuroscience, July 25, 2012]
The People's Perspective on Medicine