Wolozin Benjamin
Department of Pharmacology, Boston University School of Medicine, L-603, Boston, MA 02118-2526, USA.
Curr Opin Lipidol. 2004 Dec;15(6):667-72. doi: 10.1097/00041433-200412000-00007.
Advances in cholesterol biology suggest that cholesterol metabolism modulates beta-amyloid production, and that pharmaceuticals that inhibit cholesterol metabolism might be valuable in therapy of Alzheimer's disease. Although the genetics and cell biology continue to support the link between cholesterol and Alzheimer's disease, recent clinical studies suggest that the animal studies might not directly translate to clinical studies in humans.
This review will highlight advances in genetics, cell biology and clinical sciences investigating the relationship between cholesterol and Alzheimer's disease.
Cholesterol, its catabolites and proteins that regulate cholesterol levels all modulate processing of amyloid precursor protein. Statins hold promise in therapy of Alzheimer's disease, but the current data are more consistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-amyloid production.
胆固醇生物学的进展表明，胆固醇代谢可调节β-淀粉样蛋白的产生，抑制胆固醇代谢的药物可能对阿尔茨海默病的治疗具有重要价值。尽管遗传学和细胞生物学持续支持胆固醇与阿尔茨海默病之间的联系，但近期的临床研究表明，动物研究结果可能无法直接应用于人体临床研究。
本综述将重点介绍遗传学、细胞生物学和临床科学领域在研究胆固醇与阿尔茨海默病关系方面取得的进展。
胆固醇及其分解代谢产物以及调节胆固醇水平的蛋白质均会调节淀粉样前体蛋白的加工过程。他汀类药物有望用于治疗阿尔茨海默病，但目前的数据更符合他汀类药物作为神经保护剂而非β-淀粉样蛋白生成抑制剂的模型。
