Amyloid beta as a regulator of lipid homeostasis

被引：63

作者：

Grimm, Marcus O. W. ^{[1
]}

Grimm, Heike S. ^{[1
]}

Hartmann, Tobias ^{[1
]}

机构：

[1] Univ Saarland, D-66421 Homburg, Germany

来源：

TRENDS IN MOLECULAR MEDICINE | 2007年 / 13卷 / 08期

关键词：

D O I：

10.1016/j.molmed.2007.06.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The P-amyloid peptide (AD) is widely considered to be the molecule that causes Alzheimer's disease (AD). Besides this pathological function of AD, recently published data reveal that AD also has an essential physiological role in lipid homeostasis. Cholesterol increases AD production, and conversely AD production causes a decrease in cholesterol synthesis. The latter appears to be mediated by the inhibition of 3-hydroxy-3-methylglutaryi-coenzyme A reductase (HMGR), a key enzyme in cholesterol synthesis, in an action similar to that of statins. Moreover, AD regulates sphingolipid metabolism by directly activating sphingomyelinases (SMases). This review summarizes the molecular basis for the known physiological functions of AD and amyloid precursor protein (APP), the roles of AD and APP in lipid homeostasis and the medical implications of addressing lipid homeostasis in respect to AD. This knowledge might provide new insights for current and future therapeutic approaches to AD.

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页码：337 / 344

页数：8

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