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Tăng đáng kể β-amyloid(1–42) và protein tiền thân amyloid trong dịch não tủy não thất sau chấn thương sọ não nặng
Tóm tắt
Chấn thương sọ não nghiêm trọng (TBI) có thể dẫn đến tổn thương lan rộng tới các trục (axons), được gọi là tổn thương trục lan tỏa. Bệnh Alzheimer (AD) được đặc trưng bởi sự thoái hóa synapse và trục cùng với các mảng xơ hóa (SP). SP chủ yếu được cấu thành từ β-amyloid (Aβ) ngưng tụ, là các peptide được tạo ra từ protein tiền thân amyloid (APP). Bên cạnh việc TBI được coi là một yếu tố nguy cơ đối với AD, chấn thương đầu nặng dường như khởi phát một chuỗi sự kiện phân tử cũng liên quan đến AD. Do đó, chúng tôi đã phân tích các dạng 42 amino acid của Aβ (Aβ(1–42)) và hai dạng tan của APP (α-sAPP và ßsAPP) trong dịch não tủy não thất (VCSF) và Aβ(1–42) trong huyết tương từ 28 bệnh nhân trong mẫu liên tiếp 0–11 ngày sau TBI. Mức độ α-sAPP, ß-sAPP và Aβ(1–42) được xác định bằng phương pháp ELISA. Sau TBI, có sự gia tăng đáng kể theo từng bước của VCSF-Aβ(1–42) lên tới 1173% từ ngày 0–1 đến ngày 5–6 và sự gia tăng của VCSF-β-sAPP lên tới 2033% từ ngày 0–1 đến ngày 7–11. Cũng có một sự gia tăng nhẹ nhưng đáng kể của VCSF-β-sAPP từ ngày 0–1 đến ngày 5–6 và ngày 7–11. Ngược lại, mức độ Aβ(1–42) trong huyết tương không thay đổi sau chấn thương. Sự gia tăng rõ rệt trong VCSF-Aβ(1–42) cho thấy sự biểu hiện Aβ tăng lên có thể xảy ra như một hiện tượng thứ phát sau TBI với tổn thương trục. Mức độ không thay đổi của Aβ(1–42) trong huyết tương trái ngược với sự gia tăng rõ rệt trong VCSF-Aβ(1–42) sau chấn thương sọ não nặng, hỗ trợ gợi ý rằng Aβ(1–42) trong huyết tương không phản ánh quá trình trao đổi chất Aβ trong hệ thần kinh trung ương (CNS).
Từ khóa
#chấn thương sọ não #β-amyloid #protein tiền thân amyloid #dịch não tủy #bệnh Alzheimer #tổn thương trục lan tỏaTài liệu tham khảo
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