Prolonged changes in amyloid-β metabolism after a severe traumatic brain injury

Traumatic brain injury (TBI) is a major risk factor for Alzheimer's disease. Recent studies suggest that amyloidbeta (A beta) deposit can be detected several years after TBI. However, it is unknown whether post-TBI A beta deposits arise from short-term changes in A beta metabolism or reflect a longterm sequela. To answer this question, we evaluated the cerebrospinal levels of Aa several months after a severe TBI. The participants of this study were eight consecutive patients who developed a disorder of consciousness after a TBI, including seven in a minimally conscious state and one with unresponsive wakefulness syndrome (mean age: 35.4 +/- 14.2 years, mean time since brain injury 297.9 +/- 189.8 days). Cerebrospinal A beta(1-42) peptide was measured using a commercially available Aa enzyme-linked immunoassay kit. Reduced A beta(1-42) levels were observed in seven of eight (87.5%) patients with severe post-TBI disorders of consciousness, with the magnitude of reduction among these seven patients ranging from 27 to 75.1% of the lower normal limit. These results point to prolonged changes in A beta metabolism after a TBI and they suggest a potential mechanism of long-term neurotoxicity. NeuroReport 28: 250-252 Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved.