Michikawa Makoto
Department of Alzheimer's Disease Research, National Institute for Longevity Sciences, 36-3 Gengo, Obu, Aichi 474-8522, Japan.
Curr Alzheimer Res. 2004 Nov;1(4):271-5. doi: 10.2174/1567205043331983.
It has been suggested that a high serum cholesterol level is a risk factor for Alzheimer's disease (AD), that treatment with cholesterol-lowering drugs (statins) reduces the frequency of AD development, and that the polymorpholism of genes encoding proteins regulating cholesterol metabolism is associated with the frequency of AD development. However, the mechanism by which high serum cholesterol level leads to AD, still remains unclarified. Several recent studies have shown the results challenging the above notions. Here another notion is proposed, that is, a low high-density lipoprotein (HDL) level in serum and cerebro-spinal fluid (CSF) is a risk factor for the development of AD; moreover, the possibility that AD and Niemann-Pick type C disease share a common cascade, by which altered cholesterol metabolism leads to neurodegeneration (tauopathy) is discussed. In this review, the association between cholesterol and AD pathogenesis is discussed from different viewpoints and several basic issues are delineated and addressed to fully understand the mechanisms underlying this relationship.
有人提出,血清胆固醇水平升高是阿尔茨海默病(AD)的一个危险因素,使用降胆固醇药物(他汀类药物)治疗可降低AD发病频率,且编码调节胆固醇代谢蛋白的基因多态性与AD发病频率相关。然而,血清胆固醇水平升高导致AD的机制仍未阐明。最近的几项研究显示了与上述观点相悖的结果。在此提出另一种观点,即血清和脑脊液(CSF)中高密度脂蛋白(HDL)水平低是AD发病的一个危险因素;此外,还讨论了AD与尼曼-匹克C型病共享一个共同级联反应的可能性,即胆固醇代谢改变导致神经退行性变(tau蛋白病)。在这篇综述中,从不同角度讨论了胆固醇与AD发病机制之间的关联,并阐述和探讨了几个基本问题,以充分理解这种关系背后的机制。