gms | German Medical Science

104. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft e. V. (DOG)

21. - 24.09.2006, Berlin

How to measure neuroprotection – possible surrogate marker for neurodegeneration

Meeting Abstract

  • R. Rejdak - Department of Ophthalmology, University of Erlangen–Nurnberg, Germany
  • A. Petzold - Department of Neuroimmunology, Institute of Neurology, Queen Square, London, UK
  • K. Rejdak - Department of Neurology, Medical University of Lublin, Poland
  • T. Zarnowski - 1st Eye Hospital, Medical University of Lublin, Poland
  • A. Mankowska - 1st Eye Hospital, Medical University of Lublin, Poland
  • Z. Zagorski - 1st Eye Hospital, Medical University of Lublin, Poland
  • F. Kruse - Department of Ophthalmology, University of Erlangen–Nurnberg, Germany
  • E. Zrenner - Department of Ophthalmology, University of Tuebingen, Germany
  • A. Junemann - Department of Ophthalmology, University of Erlangen–Nurnberg, Germany

Deutsche Ophthalmologische Gesellschaft e.V.. 104. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft (DOG). Berlin, 21.-24.09.2006. Düsseldorf, Köln: German Medical Science; 2006. Doc06dogFR.11.05

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dog2006/06dog239.shtml

Veröffentlicht: 18. September 2006

© 2006 Rejdak 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 vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Degeneration of retinal axons, clinically observed as thinning of the nerve fibre layer, is associated permanent loss of vision. In many common diseases such as glaucoma, diabetic retinopathy, the functional damage may start with a small visual field defect which can progress to partial or complete blindness over time.

Over the last decades several models have been developed to study the loss of retinal axons and their ganglion cells (RGC) experimentally. With the emergence of new neuroprotective compounds these models are needed to address adequately those issues of high relevance for future clinical trials.

Biomarkers are an attractive tool for quantifying neurodegeneration. Neurofilaments can be used to specifically measure neuro-axonal loss because they are generally not expressed in other cell-types. For this reason a semi-quantitative method based RT-PCR of the mRNA of the neurofilament light chain (NfL) has been developed. This approach is logical because the amount of mRNA from the retinal tissue homogenate is likely to correlate with the number of RGC.

Our approach is based on direct quantification of a biomarker for axonal loss from the anterior chamber fluid and the vitreous body using a high throughput quantitative approach. Because of its relative biological stability and the availability of an ELISA, the phosphorylated form of the neurofilament heavy chain was the chosen biomarker.

Here we show for the first time that NfHSMI35 can be quantified from the vitreous body, but not from the anterior chamber fluid in humans. We also investigate whether the phosphorylated form of the neurofilament heavy chain (NfHSMI35), an important biomarker for axonal degeneration, could be measured from a fluid compartment of the eye.