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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

IMPACT FACTOR increased in 2015: 3.017
Rank 5 out of 30 in category Medical Laboratory Technology in the 2014 Thomson Reuters Journal Citation Report/Science Edition

SCImago Journal Rank (SJR) 2015: 0.873
Source Normalized Impact per Paper (SNIP) 2015: 0.982
Impact per Publication (IPP) 2015: 2.238

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Advanced glycation endproducts as gerontotoxins and biomarkers for carbonyl-based degenerative processes in Alzheimer's disease

Anton Rahmadi1 / Nicole Steiner1 / 1

1Department of Pharmacology, School of Medicine, University of Western Sydney, Campbelltown, Australia

Corresponding author: Associate Professor Gerald Münch, Department of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 1797, Australia Phone: +61 2 9852 4718, Fax: +61 2 9852 4730

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 49, Issue 3, Pages 385–391, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2011.079, January 2011

Publication History

Published Online:


Alzheimer's disease (AD) is the most common dementia disorder of later life. Although there might be various different triggering events in the early stages of the disease, they appear to converge on a few characteristic final pathways in the late stages, characterized by inflammation and neurodegeneration. Here, we review the hypothesis that advanced glycation end products (AGEs), which reflect carbonyl stress, an imbalance between the production of reactive carbonyl compounds and their detoxification, can serve as biomarkers for the progression of disorder. AGE modification may explain many of the neuropathological and biochemical features of AD, such as extensive protein cross-linking shown as amyloid plaques and neurofibrillary tangles, inflammation, oxidative stress and neuronal cell death. Although accumulation of AGEs is a normal feature of aging, it appears to be significantly accelerated in AD. We suggest that higher AGE concentrations in brain tissue and in cerebrospinal fluid might be able to distinguish between normal aging and AD.

Keywords: advanced glycation end products; Alzheimer's disease; carbonyl stress; gerontotoxins; methylglyoxal

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