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題 名 | 阿滋海默癡呆 (失智) 症研究近況=Alzheimer's Disease |
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作 者 | 王厚中; 江漢光; 劉文健; | 書刊名 | 醫學研究 |
卷 期 | 14:3 1993.11[民82.11] |
頁 次 | 頁141-152 |
分類號 | 415.8471 |
關鍵詞 | 癡呆症; 阿滋海默症; β類澱粉; β類澱粉前趨蛋白質; Tau蛋白; Dementia; Alzheimer's disease; β-amyloid; β-amyloid precursor protein; |
語 文 | 中文(Chinese) |
中文摘要 | 阿滋海默症是癡呆症最主要的原因之一,但其病因及致病機轉不甚清楚,且治療效果不彰。近年來的研究已有令人振奮的進展,其中以β類澱粉及β類澱粉前趨蛋白質的研究最為重要。在阿滋海默症患者腦中,β類澱粉前趨蛋白質經由異常的代謝途徑產生了大量β類澱粉的堆積,最後形成了老年斑,後者可能再間接促使神經小纖維糾結的形成。神經小纖維糾結已被証實是由tau蛋白異常的磷酸化所產生。本文就新近的研究進展做一簡介,並探討將來可行的治療策略。 |
英文摘要 | Alzheimer’s disease has been one of the major causes of dementia, but its etiology and pathogenesis have not been well revealed, rendering therapeutic efforts unsatisfactory. In the recent years there have been promising progresses in this regard. The studies of β-amyloid and β-amyloid precursor protein were among the most important ones. In the brain of patients with Alzheimer’s disease, large amount of β-amyloid accumulates via abnormal metabolism of β-amyloid precursor protein, whereby senile plaques were formed and might indirectly prectipitate the formation of neurofibrillary tangles. Neurofibrillary tangles have been shown to result from abnormal phosphorylation of tau proteins. The authors made an introduction to the recent advances in Alzheimer’s disease research and discussed some of the potential therapeutic strategies. |
本系統中英文摘要資訊取自各篇刊載內容。