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

摘要: Traumatic brain injury (TBI) is a major risk factor for Alzheimer's disease. Recent studies suggest that amyloid-beta (Aβ) deposit can be detected several years after TBI. However, it unknown whether post-TBI Aβ deposits arise from short-term changes in metabolism or reflect long-term sequela. To answer this question, we evaluated the cerebrospinal levels of months severe The participants study were eight consecutive patients who developed disorder consciousness TBI, including seven minimally conscious state and one with unresponsive wakefulness syndrome (mean age: 35.4±14.2 years, mean time since 297.9±189.8 days). Cerebrospinal Aβ1-42 peptide was measured using commercially available enzyme-linked immunoassay kit. Reduced observed (87.5%) disorders consciousness, magnitude reduction among these ranging 27 to 75.1% lower normal limit. These results point prolonged TBI they potential mechanism neurotoxicity.