Potential Blood Biomarker for TBI, and Mechanistic Link with Alzheimerâs Disease Identified
April 15, 2021
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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 teamâs work, reported in
Cell, demonstrated that traumatic brain injury (TBI) induces acetylation of the tau protein at sites that are also acetylated in human Alzheimerâs 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 ass
Researchers discover a new way to prevent brain nerve cells from deteriorating after injury
Violent blows or jolts to the head can cause traumatic brain injury (TBI), and there are currently about five million people in the U.S. living with some form of chronic impairment after suffering a TBI. 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. Behind aging and genetics, TBI is the third leading cause of Alzheimer s disease (AD), yet the link between these two conditions is not understood.
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