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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

Editorial Board Member: Gillery, Philippe / Kazmierczak, Steven / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Whitfield, John B.

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IMPACT FACTOR 2013: 2.955
Rank 5 out of 29 in category Medical Laboratory Technology in the 2013 Thomson Reuters Journal Citation Report/Science Edition

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Pentosidine determination in CSF: a potential biomarker of Alzheimer’s disease?

1 / Roberta Borghi1 / Davide Pacini1 / Carlo Serrati2 / Nicola Traverso3 / Patrizio Odetti1

1DIMI, Section of Geriatrics and Gerontology, University-Hospital IRRCS-IST San Martino, Genoa, Italy

2Neurology Unit, S. Martino University-Hospital IRRCS-IST San Martino, Genoa, Italy

3DIMES, Section of General Pathology, University of Genoa, Genoa, Italy

Corresponding author: Fiammetta Monacelli, MD, PhD, Department of Internal Medicine and Medical Specialties (DIMI), Viale Benedetto XV, 6, 16132 Genoa, Italy, Phone/Fax: +39-103537545, E-mail:

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 52, Issue 1, Pages 117–120, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/cclm-2012-0829, April 2013

Publication History

Received:
2012-11-30
Accepted:
2013-03-07
Published Online:
2013-04-06

Abstract

Background: The histopathological hallmarks in Alzheimer’s disease (AD) include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. Glycoxidation plays a crucial role in AD pathogenesis, as pentosidine and Nε- carboxymethyl-lysine (CML), were detected in AD hallmarks, and in vivo cerebrospinal fluid (CSF). However, the definitive role of AGEs in the neuropathology of AD is inconclusive. The aim of this preliminary study was to assess the level of pentosidine in CSF of patients affected by neurological disorders, including probable AD, in order to assess the feasibility of AGEs detection in CSF and to explore pentosidine as a potential biomarker in AD.

Methods: Twenty-five patients diagnosed with AD (NINCDS ADRDA criteria) and different neurological disorders were enrolled. Diabetic patients were excluded. Pentosidine, CML, amyloid β1–42 were assessed by high performance liquid chromatography (HPLC) by Odetti modified method,and by sandwich ELISA respectively.

Results: Our data showed the presence of pentosidine in all CSF samples, a significant increase in CSF pentosidine levels with age (p<0.05) and a significant decreased concentration of pentosidine in four AD subjects (p<0.01), after normalization to CSF protein concentration.

Conclusions: The study showed that AGEs concentration in CSF might benefit from age correction, at least for pentosidine, originally addressing a potential systemic age-dependent AGEs accumulation. The significant decrease of CSF pentosidine in AD, even in 4 patients, might conceive that different AGEs inform specific types of neurodegeneration, depending on oxidative stress levels, blood – brain barrier permeability, brain localization and systemic risk factors.

Keywords: Alzheimer dementia; cerebrospinal fluid (CSF); diagnosis; pentosidine

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