(dailyRx News) Traumatic brain injuries are known to be a risk factor for later development of cognitive impairments. Recent findings suggest that even a singular brain injury could lead to diminished neurological capacity.
Survivors of TBI may develop Alzheimer's-like neurodegeneration years later because such an injury may accelerate cognitive impairments, even in young adults.
Dr. Douglas Smith, professor of neurosurgery and director of the Center for Brain Injury and Repair at Penn's Perelman School of Medicine and study co-senior author, said a single TBI is very serious, potentially causing earlier development of neurodegeneration. He said this is because plaques and tangles are appearing abnormally earlier in those who previously suffered from TBI.
More than 1.7 million people in the United States suffer a TBI each year. It is an established risk factor for cognitive impairment.
Investigators found both tau tangles and amyloid-beta plaques in survivors many years after a moderate to severe TBI. Previous research has shown that the accumulation of tau is the signature of chronic traumatic encephalopathy, a degenerative disease often found in patients with multiple concussions or head injuries.
Widespread amyloid-beta plaques have been discovered in about 30 percent of patients soon after the injury, though the plaques generally disappear over the following months.
During the study, researchers examined post-mortem brains of 39 long-term survivors of a single TBI. Those patients had reported a TBI that occur between one year ago to as long ago as 47 years. The brains of those patients were compared against uninjured age-matched control subjects.
The TBI survivors showed a considerably wider distribution of tau tangles and amyloid-beta plaque pathology that was considerably more extensive than the control subjects.In about a third of cases, tangle pathology was found years after a single TBI that appeared similar to findings in patients with repetitive TBI and in neurodegenerative diseases such as Alzheimer’s disease.
In a majority of the cases investigators also found neuritic plaques, similar to senile plaques found in Alzheimer's, which suggested that years after a TBI, amyloid-beta plaques could return and accelerate neurodegeneration.
The study, which was funded by the U.S. National Institutes of Health, was published in Brain Pathology.