The long-term consequences of traumatic brain injuries are always difficult to ascertain for clients as their rehabilitation progresses. One of our concerns has always been the future risk that a client suffering from TBI would later develop Alzheimer’s or other dementias. The medical literature has not established this association to a certainty. Recent data published by the Journal of Neuroscience, however, has significantly moved forward our understanding about this significant medical risk.
Using mice and post-mortem samples from human brains, scientists from Tufts University School of Medicine have found that even a single event of moderate to severe TBI can disrupt the proteins that protect the brain from the enzymes that cause Alzheimer’s disease. Serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1, and elevation of that enzyme causes elevation of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer’s disease. It is hoped that these findings will guide future research, as well as assist in the development of future drug targets to aid in the prevention of Alzheimer’s.
Moderate to severe TBI is often caused by the significant forces found in blunt force trauma, falls, and motor vehicle accidents. The CDC has reported that over 1.7 million people suffer such injury annually, although the majority suffer a milder form of TBI called a concussion. Even concussions and repeated but lesser head trauma is suspected to lead to Alzheimer’s, however. Alzheimer’s disease is reported to affect over 5 million Americans, and is the most common cause of dementia in those over the age of 65.
Source: Depletion of GGA1 and GGA3 Mediates Postinjury Elevation of BACE1, Journal of Neuroscience, July 2012.