Active duty service members who sustain a traumatic brain injury have chronically elevated peripheral concentrations of Aβ40 and lower ratios of Aβ42/40.

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 (F = 6.948, p = 0.009) and a lower ratio of Aβ42/Aβ40 (F = 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.