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Intraneuronal advanced glycation endproducts in presenilin-1 Alzheimer's disease


The most frequently mutated gene resulting in dominantly inherited Alzheimer's disease is presenilin-1. We have used antibodies against advanced glycation endproducts (AGE) in brain tissue sections of four patients with three different presenilin I mutations. Accumulation of intracellular AGE was observed in 75-95% of pyramidal neurons in patients with presenilin-1 mutations, far exceeding the percentage of presenilin-1-, tau- or ubiquitin-positive neurons. This high level of AGE-modified proteins in vulnerable neurons is most likely explained by higher levels of their precursors (reactive (di)carbonyl products) or a slower turnover of the participating proteins. These conditions of carbonyl stress may contribute to increased neuronal dysfunction and vulnerability leading to the early disease onset.

Type Journal
ISBN 0959-4965 (Print)
Authors Munch, G.;Shepherd, C. E.;McCann, H.;Brooks, W. S.;Kwok, J. B.;Arendt, T.;Hallupp, M.;Schofield, P. R.;Martins, R. N.;Halliday, G. M. :
Publisher Name NEUROREPORT
Published Date 2002-01-01 00:00:00
Published Volume 13
Published Issue 5
Published Pages 601-4
Status Published In-print