gms | German Medical Science

81st Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

12.05. - 16.05.2010, Wiesbaden

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Accumulation of Marker Protein of DNA damage in humans of the olfactory bulb cells and spinal fluid of Alzheimer Disease Patients

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  • corresponding author Masami Rudolph - Universitätklinikum Ulm, Deutschland
  • Marc Scheithauer - HNO, Universitätklinikum Ulm, Deutschland
  • Christina von Arnim - Neurologie, Universitätklinikum Ulm, Deutschland
  • Yvonne Begus - Universität Ulm, Molecular Medicine, Ulm, Deutschland
  • J. Attems - Department of Pathology, Otto Wagner Hospital, Wien, Österreich
  • Dietmar Thal - Universität Ulm, Pathologie, Ulm, Deutschland
  • Gerhard Rettinger - HNO, Universitätklinikum Ulm, Deutschland
  • Song Zhangfa - Universität Ulm, Molecular Medicine, Ulm, Deutschland
  • Karl Lenhard Rudolph - Universität Ulm, Molecular Medicine, Ulm, Deutschland

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie. 81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie. Wiesbaden, 12.-16.05.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. Doc10hnod626

doi: 10.3205/10hnod626, urn:nbn:de:0183-10hnod6264

Published: April 22, 2010

© 2010 Rudolph et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Introduction: The diagnosis of Alzheimer disease (AD) is still challenging and biomarkers for AD remain to be developed. It has been suggested that an analysis of neurons in the olfactory epithelium could help in the diagnosis of AD. On the molecular level there is evidence that DNA damage accumulation could contribute to AD with that development.

Material and methods: Here we have investigated the level of DNA damage and telomere length in the olfactory bulb of 10 patients with AD versus 10 age-matched controls without AD. In addition, we have measured newly identified biomarkers of telomere dysfunction and DNA damage in spinal fluid of 193 AD patients and 163 controls without AD.

Results: The study shows an accumulation of DNA damage foci in olfactory bulb neurons of AD patients (32%) compared to age-matched controls (10%, p=0.06). However, there was no significant difference in telomere length in olfactory bulb neurons between the two groups. In spinal fluid a significant increase of two biomarkers of DNA damage occurred in AD patients compared to controls (Stathmin, P=0.002, Chitinese3, P<0.0001).

Conclusion: Together, these data indicate that an accumulation of telomere-independent DNA-damage is associated with AD-progression in humans. These data suggest that the analysis of DNA damage markers in spinal fluid and olfactory neurons could help to improve the diagnosis of AD. In addition, the data supports the concept that an accumulation of extreme-telomeric DNA damage contributes to the evolution of AD.