Linking lipids, Alzheimer's and LXRs?

Nuclear receptor signaling Pub Date : 2004-01-01 Epub Date: 2004-04-05 DOI:10.1621/nrs.02001
Nilay V Patel, Barry Marc Forman
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引用次数: 11

Abstract

Deposition of the beta-amyloid (Abeta) peptide is thought to underlie development of Alzheimer's disease (AD). This pathological linkage has spurred considerable interest in therapeutic strategies to reduce Abeta production. It is becoming increasingly clear that altered cholesterol homeostasis can modulate Abeta production and/or accumulation. In this review, we discuss the molecular pathology of AD, the cholesterol connection and recent data suggesting that the oxysterol receptor, liver X receptor LXR (NR1H2 and NR1H3), may modulate these events.

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脂质、阿尔茨海默病和LXRs之间的联系?
β -淀粉样蛋白(Abeta)肽的沉积被认为是阿尔茨海默病(AD)发展的基础。这种病理联系激发了对减少β产生的治疗策略的极大兴趣。越来越清楚的是,改变胆固醇稳态可以调节β的产生和/或积累。在这篇综述中,我们讨论了AD的分子病理,胆固醇的联系以及最近的数据表明,氧甾醇受体,肝脏X受体LXR (NR1H2和NR1H3)可能调节这些事件。
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