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Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and associated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer’s disease. We previously showed that  cis  phosphorylated tau ( cis  P-tau), but not the  trans  form, contributes to tau pathology and functional impairment in an animal model of severe TBI. Here we found that in human samples obtained post TBI due to a variety of causes,  cis  P-tau is induced in cortical axons and cerebrospinal fluid and positively correlates with axonal injury and clinical outcome. Using mouse models of severe or repetitive TBI, we showed that  cis  P-tau elimination with a specific neutralizing antibody administered immediately or at delayed time points after injury, attenuates the development of neuropathology and brain dysfunction during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI. Thus,  cis  P-tau contributes to short-term and long-term sequelae after TBI, but is effectively neutralized by  cis  antibody treatment.

Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae