中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2001年
2期
132-135
,共4页
Alzheimer病%钾通道%β-淀粉样蛋白%早老素
Alzheimer病%鉀通道%β-澱粉樣蛋白%早老素
Alzheimer병%갑통도%β-정분양단백%조로소
Alzheimer病目前是痴呆的最常见原因，病理学特征是：神经纤维缠结，神经斑块，神经元丢失，淀粉样血管改变。临床上最显著的特点是学习记忆障碍。钾通道在学习记忆中起着重要作用。Alzheimer病人成纤维细胞以及嗅成纤维细胞113pS四已胺敏感的钾通道缺失。记忆相关蛋白Cp20以及与Alzheimer病遗传密切相关的淀粉样蛋白前体蛋白及早老素均能调节钾通道活性。Alzheimer病时钾通道亚型的改变尚需进一步的理论研究。钾通道在Alzhe imer病治疗方面有可能成为重要靶点。
Alzheimer病目前是癡呆的最常見原因，病理學特徵是：神經纖維纏結，神經斑塊，神經元丟失，澱粉樣血管改變。臨床上最顯著的特點是學習記憶障礙。鉀通道在學習記憶中起著重要作用。Alzheimer病人成纖維細胞以及嗅成纖維細胞113pS四已胺敏感的鉀通道缺失。記憶相關蛋白Cp20以及與Alzheimer病遺傳密切相關的澱粉樣蛋白前體蛋白及早老素均能調節鉀通道活性。Alzheimer病時鉀通道亞型的改變尚需進一步的理論研究。鉀通道在Alzhe imer病治療方麵有可能成為重要靶點。
Alzheimer병목전시치태적최상견원인，병이학특정시：신경섬유전결，신경반괴，신경원주실，정분양혈관개변。림상상최현저적특점시학습기억장애。갑통도재학습기억중기착중요작용。Alzheimer병인성섬유세포이급후성섬유세포113pS사이알민감적갑통도결실。기억상관단백Cp20이급여Alzheimer병유전밀절상관적정분양단백전체단백급조로소균능조절갑통도활성。Alzheimer병시갑통도아형적개변상수진일보적이론연구。갑통도재Alzhe imer병치료방면유가능성위중요파점。
Alzheimer disease(AD) is the most common cau se of dementia today. Th e characteristic histopathologic changes include neurofibrillary tangles, neurit ic plaques, neuronal loss, and amyloid angiopathy. The noted Alzheimer symptom is the dysfunction of learning a nd memory. Potassium channels play a key role in it. A 113-pS tetraethylammoniu m-sensitive potassium channel was consistently absent from AD fibroblasts and o lfactory neuroblasts. Cp20, a memory-associated protein, amyloid precuror prote in and presenilin which are all tightly associated with genetic Alzheimer diseas e can regulate the activities of potassium channels. The changes of potassium ch annels subtype need further study. Potassium channels are maybe the important dr ug targets in the treatment of Alzheimer disease.
