Amyloid‐β and tau imaging in chronic traumatic brain injury

Background Amyloid-β and tau are the pathological hallmarks of Alzheimer’s disease. There is evidence elevated amyloid-β immediately following moderate to severe traumatic brain injury (TBI). This suggests TBI may initiate processes that lead It not clear whether remain in chronic post-injury period. To address this issue, we assessed burden long-term survivors (≥ 10 years post injury) healthy controls using PET imaging. Method Using a cross-sectional design, recruited individuals single at least previously from an inpatient rehabilitation program. A demographically similar control group was community. data were acquired 18F-NAV4694 (amyloid-β) 18F-MK6240 (tau) tracers. scans classified as positive or negative visual assessment. deposition quantified Centiloid scale. Tau standardized uptake value ratio (SUVR) four key composite regions interest (ROI). We examined relation time since age injury. analysed series regression analyses controlling for sex. Result The sample comprised 87 with (71.3% male; M = 57.53 years, SD 11.53) 59 (59% 60.34 11.97). Our results showed more likely than have scan based on Individuals did significantly higher values SUVRs any ROI. No associations identified Conclusion associated pathologies period relative controls. show significant increase Likewise, found no greater those who older their