September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Amyloid beta (Aβ) immunoreactivity in the retina of Alzheimer’s disease (AD) and non-AD dementias: A pilot study
Author Affiliations & Notes
  • Joanne A Matsubara
    Ophthalmology, University of British Columbia, Vancouver, British Columbia, Canada
  • Veronica Hirsch-Reinshagen
    Pathology, University of British Columbia, Vancouver, British Columbia, Canada
  • Ian R. Mackenzie
    Pathology, University of British Columbia, Vancouver, British Columbia, Canada
  • Robin Ging-Yuek Hsiung
    Neurology, University of British Columbia, Vancouver, British Columbia, Canada
  • Brennan Eadie
    Ophthalmology, University of British Columbia, Vancouver, British Columbia, Canada
  • Sieun Lee
    Simon Fraser University , Burnaby, British Columbia, Canada
  • Kailun Jiang
    Ophthalmology, University of British Columbia, Vancouver, British Columbia, Canada
  • Marinko Venci Sarunic
    Simon Fraser University , Burnaby, British Columbia, Canada
  • Mirza Faisal Beg
    Simon Fraser University , Burnaby, British Columbia, Canada
  • Jing Z Cui
    Ophthalmology, University of British Columbia, Vancouver, British Columbia, Canada
  • Footnotes
    Commercial Relationships   Joanne Matsubara, None; Veronica Hirsch-Reinshagen, None; Ian R. Mackenzie, None; Robin Ging-Yuek Hsiung, None; Brennan Eadie, None; Sieun Lee, None; Kailun Jiang, None; Marinko Sarunic, None; Mirza Faisal Beg, None; Jing Cui, None
  • Footnotes
    Support  Brain Canada
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 614. doi:
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      Joanne A Matsubara, Veronica Hirsch-Reinshagen, Ian R. Mackenzie, Robin Ging-Yuek Hsiung, Brennan Eadie, Sieun Lee, Kailun Jiang, Marinko Venci Sarunic, Mirza Faisal Beg, Jing Z Cui; Amyloid beta (Aβ) immunoreactivity in the retina of Alzheimer’s disease (AD) and non-AD dementias: A pilot study. Invest. Ophthalmol. Vis. Sci. 2016;57(12):614.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : AD is a devastating neurodegenerative disorder in which Aβ accumulates in the brain beyond normal limits. Assessing Aβ levels in the brain by PET imaging can confirm the presence and progression of AD, however PET imaging is costly and exposes patients to significant radiation. Retinal imaging may be a viable alternative to PET for detection of Aβ in the brain as some studies suggest that Aβ accumulates in AD retina. The purpose of this study is to assess the relationship of Aβ accumulation in the retina and brain of AD donors.

Methods : Autopsy materials from donors with a primary pathological diagnosis of AD were studied to determine the relationship of retinal and brain Aβ loads. Retina and brain of non-AD dementias (cerebral vascular disease, dementia with Lewy bodies), and retina of age-matched normals were processed for controls. Brain samples were evaluated for neuritic and diffuse senile plaques (CERAD score), Aβ protein (Thal phase), neurofibrillary tangles (Braak stage) and cerebral amyloid angiopathy. Retinal samples were processed as free floating punches (4 mm) or paraffin embedded cross sections (6µm) using mouse monoclonal Ab antibodies (6F/3D, 4G8, 6E10) and Cy3 secondary antibodies. Images were captured on a Zeiss 510 confocal microscope with LSM510 or Zen 2009 software. We analyzed labeling in the ganglion cell layer (GCL) and in the nerve fiber layer (NFL) within the central retina as well as peripheral retina (superior, inferior and temporal regions) using NIH Image J.

Results : To date, we have collected eye and brain samples from 15 donors with primary pathological diagnosis of AD and 8 donors with non-AD dementias. Pilot data from N=3 AD and N=3 non-AD dementia donors will be presented. Higher levels of Aβ were observed in the peripheral (temporal) retina compared to central retina in all 6 eyes. The Aβ immunolabeling was present in the blood vessel lumen, the neuropil, and the cytoplasm of cells in the GCL. The relationship of retinal Aβ immunoreactivity and pathological staging of AD will be discussed.

Conclusions : Aβ immunolabeling is evident in the NFL and GCL in human retina. Aβ load is higher in peripheral compared to central retina in both AD and non-AD specimens. Future studies of AD autopsy material as well as mouse models of AD will help define the relationship between the temporal and pathological deposition of Aβ protein in the brain and retina.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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