gms | German Medical Science

81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

12.05. - 16.05.2010, Wiesbaden

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

Meeting Abstract

  • 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

Veröffentlicht: 22. April 2010

© 2010 Rudolph et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

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.