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Potential Blood Biomarker for TBI, and Mechanistic Link with Alzheimer’s Disease Identified

Scientists headed by a team at the Harrington Discovery Institute have discovered a potential new approach to preventing brain nerve cells from deteriorating after brain injury. The team’s work, reported in Cell, demonstrated that traumatic brain injury (TBI) induces acetylation of the tau protein at sites that are also acetylated in human Alzheimer’s disease (AD), and revealed a potential mechanistic link between TBI and AD. The studies in addition indicated that blood levels of acetylated tau (ac-tau) could represent a potential biomarker for TBI. Strikingly, the researchers found that two FDA-approved NSAID (nonsteroidal anti-inflammatory drug) medicines, salsalate and diflunisal, were potently neuroprotective after TBI in mice, while an analysis of human records indicated that use of either drug for other indications was associated with much lower incidences of clinically diagnosed TBI, and of AD.

“This work has a number of potential clinical implications,” explained Edwin Vázquez-Rosa, PhD, co-first author on the study, which is reported in Cell. “First, it shows that the medicines salsalate and diflunisal provide previously unidentified neuroprotective activity by this new mechanism, and that in the course of being prescribed these medicine for traditional indications patients appear to also be relatively protected from developing neurodegenerative conditions. Accordingly, these medicines may also help protect TBI patients from developing AD. Finally, our work provides a new blood biomarker of neurodegeneration in the brain after TBI that could be harnessed to stage severity and progression of nerve cell deterioration after injury.”

Vázquez-Rosa and colleagues describe their findings in a paper titled, “Reducing tau acetylation is neuroprotective in brain injury.”

Violent blows or jolts to the head can cause traumatic brain injury, and there are currently about five million people in the U.S. living with some form of chronic impairment after suffering a TBI, the authors noted. Even in a mild form, TBI can lead to lifelong nerve cell deterioration associated with a wide array of neuropsychiatric conditions. Tragically, there are no medicines to protect nerve cells after injury, they wrote. “At present, treatments for TBI focus on patient stabilization and mitigation of symptoms, and there are no medicines that specifically target the pathophysiological processes that drive neurodegeneration after brain injury.” Behind aging and genetics, TBI is also the third leading cause of Alzheimer’s disease (AD), yet the link between these two conditions is not understood.

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