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β-amyloid binds to p75NTR and activates NFκB in human neuroblastoma cells

✍ Scribed by Pascal Kuner; Robert Schubenel; Cornelia Hertel

Publisher
John Wiley and Sons
Year
1998
Tongue
English
Weight
156 KB
Volume
54
Category
Article
ISSN
0360-4012

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✦ Synopsis

Amyloid ␤ peptide (A␤), a proteolytic fragment of the amyloid precursor protein (APP), is a major component of the plaques found in the brain of Alzheimer's disease (AD) patients. These plaques are thought to cause the observed loss of cholinergic neurons in the basal forebrain of AD patients. In these neurons, particularly those of the nucleus basalis of Meynert, an up-regulation of 75kD-neurotrophin receptor (p75 NTR ), a nonselective neurotrophin receptor belonging to the death receptor family, has been reported. p75 NTR expression has been described to correlate with ␤-amyloid sensitivity in vivo and in vitro, suggesting a possible role for p75 NTR as a receptor for A␤. Here we used a human neuroblastoma cell line to investigate the involvement of p75 NTR in A␤-induced cell death. A␤ peptides were found to bind to p75 NTR resulting in activation of NFB in a time-and dosedependent manner. Blocking the interaction of A␤ with p75 NTR using NGF or inhibition of NFB activation by curcumin or NFB SN50 attenuated or abolished A␤-induced apoptotic cell death. The present results suggest that p75 NTR might be a death receptor for A␤, thus being a possible drug target for treatment of AD.

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