gms | German Medical Science

23rd Annual Meeting of the German Retina Society

German Retina Society

24.09. - 25.09.2010, Freiburg

Retinal vascular pathology in a model of familial Alzheimer's disease

Meeting Abstract

  • R. Michael Dutescu - Charité, University School of Medicine Berlin, University Eye Clinic, Campus Virchow Clinic, Berlin
  • M. Baier - Robert Koch Institute, Berlin
  • I. Semkova - Charité, University School of Medicine Berlin, University Eye Clinic, Campus Virchow Clinic, Berlin
  • S. Skosyrski - Charité, University School of Medicine Berlin, University Eye Clinic, Campus Virchow Clinic, Berlin
  • N. Kociok - Charité, University School of Medicine Berlin, University Eye Clinic, Campus Virchow Clinic, Berlin
  • K.W. Rüther - Charité, University School of Medicine Berlin, University Eye Clinic, Campus Virchow Clinic, Berlin

German Retina Society. 23rd Annual Conference of the German Retina Society. Freiburg i. Br., 24.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. Doc10rg55

DOI: 10.3205/10rg55, URN: urn:nbn:de:0183-10rg559

This is the translated version of the article.
The original version can be found at: http://www.egms.de/de/meetings/rg2010/10rg55.shtml

Published: September 21, 2010

© 2010 Dutescu 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

Text

Background: Mutations of the Presenilin and Amyloid precursor protein genes are known to cause familiar Alzheimer's disease (FAD). Animal models harbouring those genes have been raised featuring the histopathological hallmarks of Alzheimer’s disease (AD) such as amyloid plaques formation, neurofibrillary tangles and neuronal loss. AD is also accompanied with vascular pathology often described as an early finding in disease progression. Focussing on ocular changes in AD, studies have shown the major hallmarks of AD, e.g β Amyloid (Aβ) deposits in retinal micro vascular walls of tgAPP/Ps1 mice. Still, there is not much known about the structural and functional changes that retinal blood vessels undergo in AD.

Methods/Results: Therefore, we investigated the vasculature in the tgAPPswe/PS1ΔE9 model of familiar Alzheimer's disease. Although gross anatomy revealed functionally comparable vascular structure, fluorescence angiograms revealed reduced peripheral retinal perfusion. Aβ positive immuno-staining present in inner retinal vessels was accompanied by para-vascular astrocyte degeneration. At 5 months of age, transgenic mice showed paravascular astrocyte degeneration. Astrocyte end feet are detached from the microvascular basal membranes. This is known to cause reduced potassium clearance from neuronal tissue, finally leading to osmotic imbalance. At 12 months, electroretinography revealed mild scotopic and photopic alterations.

Conclusions: Therefore, retinal vascular pathology is likely an early finding in AD. The easy accessibility of the retinal vascular tissue could therefore make it an efficient tool to monitor AD progression.