阿茲海默症神經影像及生物指標

目前證據顯示，阿茲海默症病理變化起始於乙型類澱粉蛋白被不正常的製造及清除，使過多乙型類澱粉蛋白類澱粉沈積腦皮質形成斑塊。斑塊接著引起神經元退化，突觸連結異常，引起失智症的症狀。近來新發展的假說認為這些病理變化可以作為生物標記偵測阿茲海默症的變化。最早在臨床症狀出現前十五年以上，就可觀察到類澱粉蛋白沈積的生物標記。與神經元退化相關的生物標記則出現較晚，但與臨床相關性較高。本文介紹五種阿茲海默症生物標記的發展，優缺點。同時針對其他發展中的阿茲海默症影像工具作個全盤性的簡介。

Current evidence supports that Alzheimer's disease (AD) was initiated when β-amyloid was abnormally processed. This was followed by formation ofβ-amyloid plaques which led to neuronal injury, synaptic dysfunction and neuronal loss. A recently developed hypothetical model of the temporal evolution of AD biomarkers proposes that five AD biomarkers depart markedly from normal in a sequential manner. Amyloid biomarkers may be found 10-15 years before the first clinical symptoms appears. Neuronal injury and degeneration biomarkers present later in the disease course but correlating better with concurrent clinical symptoms. We reviewed the development, advantage, and shortcoming of each biomarker and a brief overview of other novel imaging techniques in the research of AD.