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Lab Reports |

Antibody Therapy Blocks Effects of Traumatic Brain Injury

Tracy Hampton, PhD
JAMA. 2015;314(9):866. doi:10.1001/jama.2015.10605.
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Treating mice with an antibody against the cis form of phosphorylated tau protein (cis P-tau) can prevent some of the pathological changes that occur after traumatic brain injury (TBI), researchers report (Kondo A et al. Nature. doi:10.1038/nature14658 [published online July 15, 2015]).

Investigators at Beth Israel Deaconess Medical Center in Boston and their colleagues modeled sport- and military-related TBI in mice by exposing them to impact or blast injury. After TBI was induced in mice, the researchers observed robust and persistent elevations in cis P-tau, which caused injury to axons and disrupted axonal mitochondria and microtubule scaffolding. Subsequently, cis P-tau spread in the brain over time, leading to massive apoptotic cell death. The findings add to the investigators’ previous research showing that cis P-tau has an early pathological role in Alzheimer disease (Nakamura K et al. Cell. 2012;149[1]:232-244) and suggest that “cistauosis” may be a common early disease mechanism in TBI, chronic traumatic encephalopathy, and Alzheimer disease.

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