Active duty service members who sustain a traumatic brain injury have chronically elevated peripheral concentrations of Aß40 and lower ratios of Aß42/40.

ABSTRACT

PRIMARY OBJECTIVE: Excessive accumulation of amyloid beta (Aß) 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 Aß in younger active duty service members following a TBI. The purpose of the study was to determine if Aß 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 Aß 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 Aß40 (F1,68 = 6.948, p = 0.009) and a lower ratio of Aß42/Aß40 (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 Aß relate to TBIs and may contribute to chronic neurological symptoms.