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机构地区:[1]中山大学中山医学院解剖学教研室脑研究室,广东广州510080 [2]广州市第一人民医院内分泌科,广东广州510120
出 处:《国际内科学杂志》2007年第5期301-304,F0003,共5页International Journal of Internal Medicine
基 金:国家重点基础研究发展计划(973计划):神经变性病的机制和防治的基础研究(2006cb500700);国家自然科学基金(30470904);广东省自然科学基金(04009356);广东省科技社会发展计划项目(2006B36030003)
摘 要:在阿尔茨海默病(AD)发病机制中,占主导地位是Aβ瀑流学说:由于淀粉样前体蛋白的代谢紊乱,产生了过量的Aβ42,后者迅速聚集形成寡聚物,启动了Aβ瀑流效应,造成了Aβ的沉积,形成老年斑。越来越多的实验表明,胆固醇在Aβ的产生和异常沉积过程具有重要调节作用,同时Aβ对胆固醇调节也有反馈作用,探讨两者的相互作用和影响有助于AD发病机制的阐明。而与胆固醇代谢密切相关的因素,如载脂蛋白E、调节胆固醇代谢的药物等也成为研究的热点。The predominant theory on the pathophysiology of Alzheimer disease (AD) is the Aβ cascade theory. As a result of the mis-metabolism of amyloid precursor protein ( APP), there is an increased production of the 42 amino acid form of β-amyloid protein ( Aβ42 ) which will rapidly form oligomers that initiates a cascade of events leading to the accumulation of amyloid plaques. An increasing amount of research has confirmed that cholesterol levels modulate amyloid precursor protein and Aβsynthesis. Conversely, Aβ regulates cholesterol in a putative negative feedback loop. Discussing the association between cholesterol and Aβ will help us understand the mechanism of AD deeply. The factors which are closely associated with cholesterol, such as apolipoprotein E and the drugs modulating the cholesterol levels are also discussed.
分 类 号:R749.1[医药卫生—神经病学与精神病学]
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