TY - JOUR
T1 - Influence of advanced glycation end-products and AGE-inhibitors on nucleation-dependent polymerization of β-amyloid peptide
AU - Münch, Gerald
AU - Mayer, Samantha
AU - Michaelis, Jürgen
AU - Hipkiss, Alan R.
AU - Riederer, Peter
AU - Müller, Renate
AU - Neumann, Arne
AU - Schinzel, Reinhard
AU - Cunningham, Anne M.
PY - 1997/2/27
Y1 - 1997/2/27
N2 - Nucleation-dependent polymerization of P-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.
AB - Nucleation-dependent polymerization of P-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.
KW - β-Amyloid peptide
KW - Advanced glycation end-product
KW - AGE-inhibitor
KW - Alzheimer's disease
UR - http://www.scopus.com/inward/record.url?scp=0042207369&partnerID=8YFLogxK
U2 - 10.1016/S0925-4439(96)00062-2
DO - 10.1016/S0925-4439(96)00062-2
M3 - Article
C2 - 9061036
AN - SCOPUS:0042207369
SN - 0925-4439
VL - 1360
SP - 17
EP - 29
JO - Biochimica et Biophysica Acta. Molecular Basis of Disease
JF - Biochimica et Biophysica Acta. Molecular Basis of Disease
IS - 1
ER -