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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

Citation

Postuma, RB and Martins, RN and Cappai, R and Beyreuther, K and Masters, CL and Strickland, DK and Mok, SS and Small, DH, 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, F E B S Letters: (Federation of European Biochemical Societies), 428, (1-2) pp. 13-16. ISSN 0014-5793 (1998) [Refereed Article]


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DOI: doi:10.1016/S0014-5793(98)00475-X

Abstract

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 APP751 was a weak inhibitor of outgrowth. In substrate-bound form, both APP751 and APP695 (which does not bind to LRP) stimulated outgrowth. Thus the effect of substrate-bound APP on neurite outgrowth is not mediated by LRP.

Item Details

Item Type:Refereed Article
Keywords: Amyloid protein precursor; Heparin; Alzheimer; Apolipoprotein E; Low-density lipoprotein receptor-related protein
Research Division:Medical and Health Sciences
Research Group:Neurosciences
Research Field:Neurosciences not elsewhere classified
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Neurodegenerative Disorders Related to Ageing
Author:Small, DH (Professor David Small)
ID Code:75406
Year Published:1998
Web of Science® Times Cited:25
Deposited By:Research Division
Deposited On:2012-01-30
Last Modified:2012-02-02
Downloads:0

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