Traumatic brain injury (TBI) arises when an exterior force traumatically injures the brain. Pertaining to it, a new study from the University of Pennsylvania School of Medicine claims that the presence of a gene could foresee when TBI may lead to early symptoms of Alzheimer’s disease. Amyloid plaque deposits, known mainly for their function in Alzheimer’s disease, are apparently discovered in almost one third of people who die from severe TBI, within just hours of a brain injury and in people of all ages.
This swelling of Alzheimer’s-like deposits could be envisaged by a distinction in the gene that codes for the amyloid-busting enzyme, neprilsyin. A single traumatic brain injury (TBI) has apparently surfaced as a significant risk factor for the later growth of Alzheimer’s disease. While plaques in Alzheimer’s disease increase gradually over time and almost entirely in the elderly, similar pathology could apparently be discovered quickly following TBI.
Senior author Douglas Smith, MD, director of the Penn Center for Brain Injury and Repair and professor of Neurosurgery at the University of Pennsylvania School of Medicine, commented, “These findings may be very important for individuals at high risk of TBI, such as participants in contact sports or military personnel. A genetic screening tool may be useful in identifying those at risk of developing Alzheimer’s-like amyloid plaques following a traumatic brain injury.”
The amyoid-degrading protein, neprilysin, has supposedly been discovered in a large quantity following TBI. Difference in an individual’s capability to generate effectual neprilsyin may clarify why some people produce plaques while others do not.
Study experts observed genetic samples from 81 head-injured victims who had died following brain trauma between 4 hours and 25 days subsequent to their injuries. As anticipated, in around a third of cases, amyloid deposits were found all through the brain, akin to what is seen in early Alzheimer’s patients. The experts discovered that variations, called as polymorphisms, in part of the neprilysin gene apparently connected powerfully with the occurrence of these plaques.
Upcoming studies may examine whether these genetically predisposed individuals are the same people who go on to develop Alzheimer’s disease following TBI.
The study appeared in the Journal of Neurotrauma.