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Effects of the amyloid protein precursor of Alzheimer's disease and other ligands of the LDL receptor‐related protein on neurite outgrowth from sympathetic neurons in culture
Author(s) -
Postuma Ronald B,
Martins Ralph N,
Cappai Roberto,
Beyreuther Konrad,
Masters Colin L,
Strickland Dudley K,
Mok Su San,
Small David H
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00475-x
Subject(s) - neurite , amyloid precursor protein , ldl receptor , microbiology and biotechnology , receptor , p3 peptide , chemistry , alzheimer's disease , biochemistry , lipoprotein , in vitro , biology , medicine , cholesterol , disease
The amyloid protein precursor (APP) of Alzheimer's disease can stimulate neurite outgrowth in vitro. The receptor responsible for this effect has not been identified. Kunitz protease inhibitor (KPI)‐containing forms of APP bind to the low‐density lipoprotein receptor‐related protein (LRP). As LRP may regulate neurite outgrowth, we examined whether the effects of APP are mediated by LRP. Inhibitors of LRP decreased neurite outgrowth from chick sympathetic neurons. Most LRP ligands (α2‐macroglobulin, lactoferrin, and lipoprotein lipase) stimulated outgrowth. However, in soluble form, the KPI‐containing APP 751 was a weak inhibitor of outgrowth. In substrate‐bound form, both APP 751 and APP 695 (which does not bind to LRP) stimulated outgrowth. Thus the effect of substrate‐bound APP on neurite outgrowth is not mediated by LRP.