The latest issue of the Journal of Neuroscience (April 22, 2015) reports on animal research from the University of Kentucky which “adds to an increasing body of knowledge strongly indicating that traumatic brain injury is a contributor to increased susceptibility to Alzheimer’s Disease-relevant pathologies, including cognitive dysfunction.”
The authors begin by noting that “epidemiological studies have associated increased risk of Alzheimer’s disease-related clinical symptoms with a medical history of head injury,” but that “little is known about the pathophysiological mechanisms linked to this association.” Prior studies, as well as this study, did find that persistent neuroinflammation is one outcome observed in patients after a single head injury.
The first conclusion in this study is that
“a single, comparatively mild, diffuse brain injury administered before onset of age-associated functional deficits and pathology in an AD-relevant mouse model can induce chronic cognitive impairment.”
Similar neuroinflammation has also been found to be present early in relevant brain regions during the Alzheimer’s disease progression. Animal studies models have linked neuroinflammation to neuropathology and cognitive impairment in both brain injury and Alzheimer’s disease.
The authors explored the potential interplay between these two pathologies in hopes of making progress towards a treatment that might interrupt the process that links the two conditions. The results of the study laid a foundation for developing such a treatment. To explore the chain of events that link TBI to dementia, the authors used mice that were genetically altered to make a human protein called amyloid beta, a key player in Alzheimer’s disease. The mice were then subjected to a procedure that mimics a mild traumatic brain injury. Some of the mice received a small molecule drug known as MW151, which blocks overproduction of the molecules that cause inflammation in the brain following TBI. The mice that received this treatment no longer showed learning and memory problems, while the mice that didn’t receive the drug showed profound learning and memory problems.
The implications of this work regarding a link between TBI and Alzheimers cannot be overstated, as the authors note in a recent story on the research in ScienceDaily:
“As the signature injury of the Iraq and Afghanistan wars, and with approximately 1.5 million people in the United States each year seeking medical treatment for a traumatic brain injury, the impact of earlier onset of dementia in such a large number of people is simply unthinkable…Adam and Scott’s work could have a large impact both socially and economically.”