One traumatic brain injury (TBI) can keep on damaging the brain nerves for many years, according to a new study carried out by Perelman School of Medicine at the University of Pennsylvania. The researchers said that apart from the immediate effects of single TBI, neurodegeneration can result which is much like that of Alzheimer’s disease. Even young adults were not immune from the risk.
More than 1.7 million Americans suffer from traumatic brain injury every year and growing evidence suggests that brain damaging processes can be initiated after that. TBI is already established as a risk factor for development of cognitive disabilities later on in life. The serious health concerns due to even a single TBI is both immediate and long-term as harmful plaques and tangles show up unusually early in life, according to the study's senior author, Douglas Smith, MD, professor of Neurosurgery and director of the Center for Brain Injury and Repair at Penn's Perelman School of Medicine.
The researchers found that tau tangles and amyloid-beta tangles appear in survivors years after the incident which caused severe to moderate TBI. In the study, 39 long-term survivors of single TBI were examined for brain damage and compared with uninjured people. The time after survival of those being examined ranged from 1 to 47 years. TBI survivors were found to have a high density and broad distribution of neurofibrillary tau tangles and amyloid-beta plaque pathology, indicators of neurodegeneration. This was not found in the controls.
One-third of the TBI survivors under observation had something more to reveal. It was found that they show tangle pathology similar to that found in cases of repetitive TBI and Alzheimer’s disease. The characteristics of amyloid-beta plaques were found to be similar to the “senile” plaques found in patients of Alzheimer’s disease. A disturbing finding was that years after even a single TBI, these plaques can become like those found in the disease.
These two pathological findings suggest that there is a link between even a single TBI and increased risk of Alzheimer’s disease. This research paves the way for a better understanding of the long-term process of neurodegenration after a single TBI which can help in development of a cure. In future researches based on these findings, it is hoped that critical targets can be identified for treatment with the help of emerging anti-tau and anti-amyloid therapies.
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