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Clinical Chemistry and Laboratory Medicine (CCLM)

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

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Volume 52, Issue 1 (Jan 2014)


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

Fiammetta Monacelli
  • Corresponding author
  • DIMI, Section of Geriatrics and Gerontology, University-Hospital IRRCS-IST San Martino, Genoa, Italy
  • Email:
/ Roberta Borghi
  • DIMI, Section of Geriatrics and Gerontology, University-Hospital IRRCS-IST San Martino, Genoa, Italy
/ Davide Pacini
  • DIMI, Section of Geriatrics and Gerontology, University-Hospital IRRCS-IST San Martino, Genoa, Italy
/ Carlo Serrati
  • Neurology Unit, S. Martino University-Hospital IRRCS-IST San Martino, Genoa, Italy
/ Nicola Traverso
  • DIMES, Section of General Pathology, University of Genoa, Genoa, Italy
/ Patrizio Odetti
  • DIMI, Section of Geriatrics and Gerontology, University-Hospital IRRCS-IST San Martino, Genoa, Italy
Published Online: 2013-04-06 | DOI: https://doi.org/10.1515/cclm-2012-0829


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


  • 1.

    Thorpe SR, Baynes JW. Role of the Maillard reaction in diabetes mellitus and diseases of aging. Drugs Aging 1996;9:69–77.

  • 2.

    Finch CE, Cohen DM. Aging, metabolism, and Alzheimer disease: review, and hypotheses. Exp Neurol 1997;143:82–102.

  • 3.

    Castellani RJ, Perry G, Harris PL, Monnier VM, Cohen ML, Smith MA. Advanced glycation modification of Rosenthal fibers in patients with Alexander disease. Neurosci Lett 1997;231:79–82.

  • 4.

    Horie K, Myata T, Yasuda T, Takeda A, Yasuda Y, Maeda K, et al. Immunohistochemical localization of advanced glycation end products, pentosidine, and carboxymethyllysine in lipofuscin pigments of Alzheimer’s disease and aged neurons. Biochem Biophys Res Commun 1997;236:327–32.

  • 5.

    Serot J-M, Bene MC, Foliguet B, Faure GC. Morphological alterations of the choroid plexus in late-onset Alzheimer’s disease. Acta Neuropathol (Berl) 2000;99:105–8.

  • 6.

    Ahmed N, Ahmed U, Thornalley PJ, Hager K, Fleischer G, Münch G. Protein glycation, oxidation and nitration adduct residues and free adducts of cerebrospinal fluid in Alzheimer’s disease and link to cognitive impairment. J Neurochem 2005;92: 255–63.

  • 7.

    McKahnn G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s disease. Neurology 1984;34:939–44.

  • 8.

    Odetti P, Fogarty J, Sell DR, Monnier VM. Chromatographic quantitation of plasma and erythrocyte pentosidine in diabetic and uremic subjects. Diabetes 1992;4:153–9.

  • 9.

    Tapiola T, Alafuzoff I, Herukka SK, Parkkinen L, Hartikainen P, Soininen H, et al. Cerebrospinal fluid β-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain. Arch Neurol 2009;66:382–9.

  • 10.

    Bar KJ, Franke S, Wenda B, Muller S, Kientsch-Engel R, Stein G. Pentosidine and N-ε-(carboxymethyl)-lysine in Alzheimer’s disease and vascular dementia. Neurobiol Aging 2003;24: 333–8.

About the article

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:

Received: 2012-11-30

Accepted: 2013-03-07

Published Online: 2013-04-06

Published in Print: 2014-01-01

Citation Information: Clinical Chemistry and Laboratory Medicine, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: https://doi.org/10.1515/cclm-2012-0829. Export Citation

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