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Influence of advanced glycation end-products and AGE-inhibitors on nucleation-dependent polymerization of beta-amyloid peptide

Abstract

Nucleation-dependent polymerization of beta-amyloid peptide, the major component of plaques in patients with Alzheimer's disease, is significantly accelerated by crosslinking through Advanced Glycation End-products (AGEs) in vitro. During the polymerization process, both nucleus formation and aggregate growth are accelerated by AGE-mediated crosslinking. Formation of the AGE-crosslinked amyloid peptide aggregates could be attenuated by the AGE-inhibitors Tenilsetam, aminoguanidine and carnosine. These experimental data, and clinical studies, reporting a marked improvement in cognition and memory in Alzheimer's disease patients after Tenilsetam treatment, suggest that AGEs might play an important role in the etiology or progression of the disease. Thus AGE-inhibitors may generally become a promising drug class for the treatment of Alzheimer's disease.

Type Journal
ISBN 0006-3002 (Print)
Authors Munch, G.;Mayer, S.;Michaelis, J.;Hipkiss, A. R.;Riederer, P.;Muller, R.;Neumann, A.;Schinzel, R.;Cunningham, A. M. :
Publisher Name BBA-MOL BASIS DIS
Published Date 1997-01-01 00:00:00
Published Volume 1360
Published Issue 1
Published Pages 17-29
URL http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9061036
Status Published In-print