Canevari Laura, Clark John B
Miriam Marks Division of Neurochemistry, Department of Molecular Neuroscience, Institute of Neurology, University College London, Queen Square, London, UK.
Neurochem Res. 2007 Apr-May;32(4-5):739-50. doi: 10.1007/s11064-006-9200-1. Epub 2006 Dec 27.
Since the discovery of the significance of the cholesterol-carrying apolipoprotein E and cholesterolaemia as major risk factors for Alzheimer's Disease (AD) there has been a mounting interest in the role of this lipid as a possible pathogenic agent. In this review we analyse the current evidence linking cholesterol metabolism and regulation in the CNS with the known mechanisms underlying the development of Alzheimer's Disease. Cholesterol is known to affect amyloid-beta generation and toxicity, although it must be considered that the results studies using the statin class of drugs to lower plasma cholesterol may be affected by other effects associated with these drugs. Finally, we report some of our results pointing at the interplay between neurons and astrocytes and NADPH oxidase activation as a new candidate mechanism linking cholesterol and AD pathology.
自从发现携带胆固醇的载脂蛋白E和胆固醇血症作为阿尔茨海默病(AD)的主要危险因素的重要性以来,人们对这种脂质作为可能的致病因子的作用越来越感兴趣。在这篇综述中,我们分析了目前将中枢神经系统中胆固醇代谢和调节与阿尔茨海默病发展的已知机制联系起来的证据。已知胆固醇会影响β-淀粉样蛋白的生成和毒性,不过必须考虑到,使用他汀类药物降低血浆胆固醇的研究结果可能会受到这些药物相关的其他效应的影响。最后,我们报告了一些研究结果,这些结果表明神经元与星形胶质细胞之间的相互作用以及NADPH氧化酶激活是将胆固醇与AD病理联系起来的一种新的候选机制。