Citation

Lejbman N, Olivera A, Heinzelmann M, Feng R, Yun S, Kim HS, Gill J. Brain Inj. 2016; 30(12): 1436-1441.

Affiliation

a National Institute of Nursing Research, National Institutes of Health , Bethesda , MD , USA.

Copyright

(Copyright © 2016, Informa - Taylor and Francis Group)

DOI

10.1080/02699052.2016.1219054

PMID

27834544

Abstract

PRIMARY OBJECTIVE: Excessive accumulation of amyloid beta (Aβ) and tau have been observed in older individuals with chronic neurological symptoms related to a traumatic brain injury (TBI), yet little is known about the possible role of Aβ in younger active duty service members following a TBI. The purpose of the study was to determine if Aβ 40 or 42 related to sustaining a TBI or to chronic neurological symptoms in a young cohort of military personnel. RESEARCH DESIGN: This was a cross-sectional study of active duty service members who reported sustaining a TBI and provided self-report of neurological and psychological symptoms and provided blood.

METHODS AND PROCEDURES: An ultrasensitive single-molecule enzyme-linked immunosorbent assay was used to compare concentrations of Aβ in active duty service members with (TBI+; n = 53) and without (TBI-; n = 18) a history of TBI. Self-report and medical history were used to measure TBI occurrence and approximate the number of total TBIs and the severity of TBIs sustained during deployment. MAIN OUTCOMES AND RESULTS: This study reports that TBI is associated with higher concentrations of Aβ40 (F1,68 = 6.948, p = 0.009) and a lower ratio of Aβ42/Aβ40 (F1,62 = 5.671, p = 0.020). These differences remained significant after controlling for co-morbid symptoms of post-traumatic stress disorder and depression.

CONCLUSIONS: These findings suggest that alterations in Aβ relate to TBIs and may contribute to chronic neurological symptoms.

Language: en