A new study, conducted by researchers from the Mario Negri Institute for Pharmacological Research of Milan and the University of Glasgow, has found that a single traumatic brain injury (TBI) could help trigger an abnormal form of dementia associated with protein tau.
Tau, a form of proteins in the body, when in excess levels, has been responsible for the development of neurodegenerative diseases like Alzheimer’s and Parkinson’s disease. Researchers believe inhibiting tau may provide beneficiary effects.
For the study, the team of researchers examined brain specimens of 15 patients, aged 19 to 89, who experienced a severe traumatic brain injury within a year or more. The specimens were then compared with a counterpart with no known history of brain injury.
Researchers quickly found evidence of widespread deposits of tau proteins in the brain of injured patients. The presence of tau was significantly higher compared to the healthy counterpart. In previous studies, researchers have been able to uncover similar findings of abnormal tau in the injured brains of mice.
“In parallel studies we observed the same type of abnormal tau in injured mice, which, over time, spread from the site of injury to involve remote brain regions. This progressive spread of tau was reminiscent of the spreading of prions, the infectious proteins more commonly associated with diseases such as CJD.”
The results, according to researchers, provide the first evidence linking brain injury to widespread tau deposition in humans, in addition to a self-propagating form of tau in mice. The long-term effects of tau propagation may induce the development of a degenerative disease.
“This observation that a single brain trauma is associated with widespread tau deposition in humans and to the formation of a self-propagating form of tau in a relevant animal model provides the first evidence for how a mechanical brain injury might evolve into chronic degenerative brain disease, including CTE.”
The findings were published in the journal Brain.
