Citation

Pattinson CL, Gill JM, Lippa SM, Brickell TA, French LM, Lange RT. J. Trauma. Stress 2019; 32(4): 546-554.

Affiliation

University of British Columbia, Vancouver, British Columbia, Canada.

Copyright

(Copyright © 2019, International Society for Traumatic Stress Studies, Publisher John Wiley and Sons)

DOI

10.1002/jts.22418

PMID

31291489

Abstract

Concurrent mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD) are common in U.S. military service members and veterans. Tau and amyloid-beta-42 (Aβ42) are proteins that have been linked to cognitive impairment, neurological hallmarks of Alzheimer's disease, and may also relate to recovery from mTBI. However, the role of these proteins in the maintenance or resolution of chronic symptoms has not yet been determined. Participants in the current study were 102 service members and veterans who had sustained an mTBI (n = 84) or injured controls (IC) without TBI (n = 18). They were categorized into three groups based on the presence or absence of mTBI and PTSD: IC/PTSD-Absent (n = 18), mTBI/PTSD-Absent (n = 63), and mTBI/PTSD-Present (n = 21). Concentrations of tau and Aβ42 in peripheral blood plasma were measured using Simoa^TM , an ultrasensitive technology, and compared across groups. Tau concentrations were highest in the mTBI/PTSD-Present group, F(2, 99) = 4.33, p =.016, compared to the other two groups. Linear multiple regression was conducted to determine the independent effects of PTSD and mTBI on tau concentrations, controlling for gender and sleep medication. PTSD was a significant and independent predictor of tau concentrations, β =.25, p =.009, η_p² =.26. Aβ42 concentrations did not differ between the groups. The results indicated that PTSD was associated with an elevation of tau in peripheral blood and suggest that there may be increased biological effects of PTSD in this young cohort of service members and veterans following mTBI.

© 2019 International Society for Traumatic Stress Studies.

Language: en