September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Nonvascular Retinal Imaging Markers of Preclinical Alzheimer’s Disease
Author Affiliations & Notes
  • Cláudia Yang Santos
    Interdisciplinary Neuroscience Program, University of Rhode Island, Providence, Rhode Island, United States
    Lifespan-Rhode Island Hospital, Clinical Research Center, Providence, Rhode Island, United States
  • Lenworth N Johnson
    Department of Neuro-Ophthalmology , Warren Alpert Medical School of Brown University, Providence, Rhode Island, United States
    Lifespan-Rhode Island Hospital, Clinical Research Center, Providence, Rhode Island, United States
  • Jessica L Alber
    Department of Neurology, Warren Alpert Medical School of Brown University, Providence, Rhode Island, United States
    Lifespan-Rhode Island Hospital, Clinical Research Center, Providence, Rhode Island, United States
  • Brian Fernandez
    Heidelberg Engineering, Inc, Franklin, Massachusetts, United States
  • Yen Ying Lim
    The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia
  • Peter J Snyder
    Department of Neurology, Warren Alpert Medical School of Brown University, Providence, Rhode Island, United States
    Lifespan-Rhode Island Hospital, Clinical Research Center, Providence, Rhode Island, United States
  • Footnotes
    Commercial Relationships   Cláudia Santos, None; Lenworth Johnson, None; Jessica Alber, None; Brian Fernandez, None; Yen Lim, None; Peter Snyder, None
  • Footnotes
    Support  Supported by unrestricted research grant from Pfizer Inc. to Dr. Peter J.Snyder.
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5987. doi:
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    • Get Citation

      Cláudia Yang Santos, Lenworth N Johnson, Jessica L Alber, Brian Fernandez, Yen Ying Lim, Peter J Snyder; Nonvascular Retinal Imaging Markers of Preclinical Alzheimer’s Disease. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5987.

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

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Abstract

Purpose : Successful treatment of Alzheimer’s disease (AD) requires early detection. It is known that individuals with symptomatic AD have beta-amyloid (Aβ) plaques in the brain and concomitant accumulation of Aβ plaques in the retina.1,2 In the preclinical stage of AD there is accumulation of neocortical Aβ plaques. The aim of this study was to characterize early structural retinal changes in preclinical AD.

Methods : Sixty-three adults aged 55-75 with a self-reported first degree family member with AD and subjective memory complaint underwent 18F-florbetapir PET to quantify the degree of neocortical Aβ accumulation. Neocortical PET standardized uptake value ratio (SUVr) were summed and normalized to the whole cerebellum. Participants underwent spectral-domain optical coherence tomography (OCT) including blue laser autofluorescence (BAF) imaging (Heidelberg SPECTRALIS system) to identify retinal Aβ plaque inclusion bodies and measure retinal layer thickness.

Results : The values of PET SUVr, the surface area of Aβ plaque inclusion bodies, and the thickness of the inner plexiform layer (IPL) are provided in the Figures 1 and 2. There was a moderate correlation (r= 0.46, p=0.02) between PET neocortical amyloid burden and the surface area of inclusion bodies (Figure 1), and moderate correlation (r= 0.41, p=0.03) between the surface area of inclusion bodies and an increase in the thickness of the IPL – but not for other retinal neuronal layers (Figure 2).

Conclusions : The positive correlation between the surface area of inclusion bodies in the retina and amyloid aggregation in the neocortex suggests that BAF might allow for visualization of the fibrillary form of Aβ in preclinical AD subjects. The IPL is a cholinergic rich layer in the vertebrate retina3, and early cholinergic changes in preclinical disease appear to co-occur with the onset of amyloid deposit in the major cholinergic centers of the brain. 4-6 OCT imaging of these early neuropathic changes in the retina may provide biomarkers that are both indicative of disease burden and progression and also reflective of time-specific changes in the neocortex.

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

 

 

Aβ+ CN older adult: example of inclusion bodies around vessel walls, and in peripheral regions of the retina.

Aβ+ CN older adult: example of inclusion bodies around vessel walls, and in peripheral regions of the retina.

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