What is it about?

This is the first demonstration that chronic neurodegeneration and associated cognitive impairment in chronic TBI can be reversed, even when treatment is initiated long after the acute injury. This highly-powered study applied a model of multimodal TBI that represents aspects of the major causes of TBI in people (concussive impact, acceleration / deceleration, and early blast wave exposure). Treatment of mice for just one month with the aminopropyl carbazole P7C3-A20, initiated one year after TBI (the equivalent of decades in people), restored cognitive function and arrested chronic axonal degeneration in mice. P7C3-A20 facilitated repair of endothelial cells of the blood brain barrier, which could explain why brief treatment led to lasting benefits months later.

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Why is it important?

Traumatic brain injury (TBI) causes chronic neurodegeneration and cognitive impairment, and TBI is now considered a chronic health condition. It has long been assumed that the chronic neurodegeneration-driven long-term deficits of TBI cannot be reversed. This study, however, points to therapeutic protection of the blood-brain barrier (BBB) as a therapeutic target for this goal, offering new hope to patients and their care providers for normalization of cognitive function.

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This page is a summary of: P7C3-A20 treatment one year after TBI in mice repairs the blood–brain barrier, arrests chronic neurodegeneration, and restores cognition, Proceedings of the National Academy of Sciences, October 2020, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2010430117.
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