阿茲海默氏症知能之藥物治療

Current Treatment of Cognition in Alzheimer’s Disease

阿茲海默氏症（簡稱阿症）知能之藥物治療的研發近十年來進展快速，由無到目前有許多藥物可供選擇。阿症知能的治療分三個層次：症狀改善、延緩病程及根治或預防。目前還是處於症狀改善的階段，而以乙醯膽鹼抑制劑為治療的主流。根據嚴謹的隨機雙盲臨床試驗結果，美國食品藥物管理局已通過tacrine、donepezil和rivastigmine三種乙醯膽鹼抑制劑。一般而言，這些藥物只對三分之一左右的輕度到中度阿症患者的知能稍有改善。可能延緩病程的藥物包括抗氧化物、女性荷爾蒙及抗消炎藥物。這些藥物雖有流行病學及小規模臨床試驗的資料顯示可能有延緩病程的效果，但還不能廣泛臨床使用。根治或預防阿症主要在抑制患者腦內類澱粉斑的形成，而類澱粉是由澱粉前身蛋白經由β及γ分泌酵素切割而來。1999年已有學者找出β分泌酵素的基因及蛋白，將來就可針對此蛋白研發出抑制劑，以預防阿症了。

Pharmacological treatment of cognition in Alzheimer’s disease (AD) has been advanced in recent years. There are three aspects of treatment of AD: symptomatic treatment, delaying course and curative or preventive treatment. At present, pharmacological treatment of AD is still in the stage of symptomatic, mainly cholinesterase inhibitors. The FDA of the U.S. has approved three cholinesterase inhibitors: tacrine, donepezil and rivastigmine. In general, these agents improve the cognition in about one-third of AD patients. Drugs that have been proposed in delaying the course of AD include antioxidants, estrogen and anti-inflammatory drugs. One way to cure the AD is to prevent the formation of β-amyloid, one of the main pathological findings in the brain of AD patients. β-amyloid is a product of amyloid precursor protein (APP) after being cleaved byβand γsecretases. In 1999, several investigators have found the gene and protein of β-site APP-cleaving enzyme. These findings might lead the scientists to develop the drugs preventing the formation of amyloid in the future.