Journal
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Volume 20, Issue 2, Pages 191-200Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2008.10.005
Keywords
Lipoprotein receptors; Cholesterol; Amyloid precursor protein; Amyloid-beta peptide; Alzheimer's disease
Categories
Funding
- National Institutes of Health
- Alzheimer's Association
- American Health Assistance Foundation
- Fondo de Investigacion Avanzada en Areas Prioritarias (FONDAP) [13980001]
- Millenium Institute for Fundamental and Applied Biology (MIFAB)
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Amyloid-beta (A beta) peptide accumulation in the brain is central to the pathogenesis of Alzheimer's disease (AD). A beta is produced through proteolytic processing of a transmembrane protein, beta-amyloid precursor protein (APP), by beta- and gamma-secretases. Mounting evidence has demonstrated that alterations in APP cellular trafficking and localization directly impact its processing to A beta. Members of the low-density lipoprotein receptor family, including LRP, LRP1B, SorLA/LR11, and apoER2, interact with APP and regulate its endocytic trafficking. Additionally, APP trafficking and processing are greatly affected by cellular cholesterol content. In this review, we summarize the current understanding of the roles of lipoprotein receptors and cholesterol in APP trafficking and processing and their implication for AD pathogenesis and therapy. (C) 2008 Elsevier Ltd. All rights reserved.
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