Fig. 2

Cis P-tau in the CSF of severe TBI patients is neurotoxic and correlates with clinical outcome at 1 year after injury. a Detection of cis P-tau in the CSF of a TBI patient was performed by subjecting control CSF or CSF specimens collected from EVD at different times after TBI due to jumping into an oncoming train to immunoprecipitation with cis mAb, followed by immunoblotting with rabbit anti-tau mAb (top panel) or to direct ELISA with cis mAb in OD at 450 nm (bottom panel). Post-mortem Alzheimer’s patient CSF (AD) and control CSF were used as positive and negative controls, respectively. b, c Addition of TBI CSF to neurons induces dose-dependent cell death in recipient cells, which are fully rescued by immunodepletion with cis, but not trans mAb. Human control and TBI CSF specimens were added to culture media of SY5Y neurons for 3 days, followed by the live (green)/dead (red, white arrows) cell assay. For immunodepletion, cis or trans mAb was incubated with TBI CSF to deplete cis or trans p-tau before adding to cells. n = 3. d, e Cis P-tau levels of CSFs taken day 4 to 6 days after injury of acute TBI patients were measured by direct ELISA and an ordered logistic regression was used to model 1 year GOS as the outcome and cis P-tau level in OD at 450 nm as the main predictor, controlling for age, gender and initial Glasgow Coma Scale. Supplementary Table 2 shows demographic information for the subjects. n = 20