Researchers at the University of Pennsylvania School of Medicine have shown for the first time that a single traumatic brain injury (TBI) may initiate or accelerate long-term neurodegeneration, even in young adults.
TBI is an established risk factor for later development of cognitive impairments, such as Alzheimer's disease.
A single traumatic brain injury is very serious, both initially, and as we're now learning, even later in life, said Douglas Smith, MD, professor of Neurosurgery and director of the Center for Brain Injury and Repair at Penn's Perelman School of Medicine, the study's co-senior author.
Plaques and tangles are appearing abnormally early in life, apparently initiated or accelerated by a single TBI, he added.
The study, done in conjunction with neuropathologist Dr. William Stewart, from the University of Glasgow and Southern General Hospital in Glasgow, UK, found both tau tangles and amyloid-beta plaques in survivors, years after a single moderate-to-severe TBI.
In repetitive head injury, previous studies have shown a tau accumulation as the signature pathology of a condition called chronic traumatic encephalopathy.
In this study, the researchers examined post-mortem brains from 39 long-term survivors of a single TBI, extending the survival time from 1-47 years survival after TBI, and compared them to uninjured, age-matched controls.
TBI survivors showed a high density and wide distribution of neurofibrillary tau tangles and amyloid-beta plaque pathology far beyond what was found in controls.
Specifically, about a third of the cases showed tangle pathology years after a single TBI, similar in appearance to the tangles found after repetitive TBI and in neurodegenerative diseases such as Alzheimer's disease.
Moreover, the amyloid-beta plaques were not only found years after TBI, but the majority of cases displayed diffuse as well as "neuritic" plaques with the same character as "senile" plaques also found in Alzheimer's disease. This suggests that years after a single TBI, amyloid-beta plaques may return and become neuritic.
The study appears online in Brain Pathology.