A recent study conducted by the Perelman School of Medicine at the University of Pennsylvania reveals that a single traumatic brain injury (TBI) can continue to harm brain nerves over many years. The research suggests that beyond the immediate effects of a single TBI, neurodegeneration similar to that seen in Alzheimer’s disease can occur. Even young adults are not exempt from this risk.
Each year, more than 1.7 million Americans suffer from traumatic brain injuries, and mounting evidence indicates that processes damaging the brain can persist afterward. TBIs are already recognized as a risk factor for cognitive disabilities later in life. The study’s senior author, Dr. Douglas Smith, highlights the dual health concerns associated with even a single TBI, as harmful plaques and tangles appear unusually early in life.
The researchers discovered that survivors of single TBIs exhibited tau tangles and amyloid-beta plaques years after the initial injury, indicative of neurodegeneration. In a study involving 39 long-term survivors, ranging from 1 to 47 years post-injury, individuals with TBI displayed a high density and wide distribution of these pathological markers compared to uninjured individuals.
Furthermore, one-third of the TBI survivors examined exhibited tangle pathology similar to that seen in cases of repetitive TBI and Alzheimer’s disease. The characteristics of amyloid-beta plaques resembled those found in Alzheimer’s patients, suggesting that even years after a single TBI, these plaques can resemble those in the disease.
These findings suggest a link between a single TBI and an increased risk of Alzheimer’s disease. The research lays the groundwork for better understanding the long-term process of neurodegeneration following a single TBI, potentially aiding in the development of a cure. Future research based on these findings aims to identify critical treatment targets using emerging anti-tau and anti-amyloid therapies.