Amyloid beta as a regulator of lipid homeostasis |
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| Authors: | Grimm Marcus O W Grimm Heike S Hartmann Tobias |
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| Institution: | 1. Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada;2. Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX 77030, USA;3. Research Center on Aging, Department of Physiology and Biophysics, University of Sherbrooke, Sherbrooke, Quebec J1H 5N4, Canada;4. Genzyme, a Sanofi Company, Framingham, MA 01701, USA;5. Translational Laboratory in Genetic Medicine, Agency for Science, Technology and Research, 138648, Singapore;6. Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, 138648, Singapore |
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| Abstract: | The beta-amyloid peptide (A beta) is widely considered to be the molecule that causes Alzheimer's disease (AD). Besides this pathological function of A beta, recently published data reveal that A beta also has an essential physiological role in lipid homeostasis. Cholesterol increases A beta production, and conversely A beta production causes a decrease in cholesterol synthesis. The latter appears to be mediated by the inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), a key enzyme in cholesterol synthesis, in an action similar to that of statins. Moreover, A beta regulates sphingolipid metabolism by directly activating sphingomyelinases (SMases). This review summarizes the molecular basis for the known physiological functions of A beta and amyloid precursor protein (APP), the roles of A beta 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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