The generation and function of soluble apoE receptors in the CNS

G William Rebeck¹ , Mary Jo LaDu² , Steven Estus³^,4 , Guojun Bu⁵^,6^,7 and Edwin J Weeber⁸^,9^,10

¹Department of Neuroscience, Georgetown University, Washington DC, USA

²Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, USA

³Department of Physiology, University of Kentucky, Lexington, USA

⁴Sanders-Brown Center on Aging, University of Kentucky, Lexington, USA

⁵Department of Pediatrics, Washington University, St. Louis, USA

⁶Department of Cell Biology and Physiology, Washington University, St. Louis, USA

⁷Hope Center for Neurological Disorders, Washington University, St. Louis, USA

⁸Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, USA

⁹Department of Pharmacology, Vanderbilt University, Nashville, USA

¹⁰Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, USA

author email corresponding author email

Molecular Neurodegeneration 2006, 1:15doi:10.1186/1750-1326-1-15


Published:	24 October 2006

Abstract

More than a decade has passed since apolipoprotein E4 (APOE-ε4) was identified as a primary risk factor for Alzheimer 's disease (AD), yet researchers are even now struggling to understand how the apolipoprotein system integrates into the puzzle of AD etiology. The specific pathological actions of apoE4, methods of modulating apolipoprotein E4-associated risk, and possible roles of apoE in normal synaptic function are still being debated. These critical questions will never be fully answered without a complete understanding of the life cycle of the apolipoprotein receptors that mediate the uptake, signaling, and degradation of apoE. The present review will focus on apoE receptors as modulators of apoE actions and, in particular, explore the functions of soluble apoE receptors, a field almost entirely overlooked until now.