June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Retinal image analysis and Alzheimer's disease
Author Affiliations & Notes
  • Imre Lengyel
    Ocular Biology and Therapeutics, UCL Institute of Ophthalmology, London, United Kingdom
  • Nicola B Quinn
    Queen's University, Belfast, United Kingdom
  • Lajos Csincsik
    Ocular Biology and Therapeutics, UCL Institute of Ophthalmology, London, United Kingdom
  • Craig Ritchie
    University of Edinburgh, Edinburgh, United Kingdom
  • Ruth E Hogg
    Queen's University, Belfast, United Kingdom
  • Sebastian Crutch
    Dementia Research Centre, London, United Kingdom
  • Tunde Peto
    Depaetment of Research and Development, Moorfields Eye Hospital, London, United Kingdom
  • Timothy Shakespeare
    Dementia Research Centre, London, United Kingdom
  • Footnotes
    Commercial Relationships Imre Lengyel, OPTOS (F); Nicola Quinn, None; Lajos Csincsik, OPTOS (F); Craig Ritchie, None; Ruth Hogg, OPTOS (F); Sebastian Crutch, None; Tunde Peto, OPTOS (F); Timothy Shakespeare, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2795. doi:
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      Imre Lengyel, Nicola B Quinn, Lajos Csincsik, Craig Ritchie, Ruth E Hogg, Sebastian Crutch, Tunde Peto, Timothy Shakespeare; Retinal image analysis and Alzheimer's disease. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2795.

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

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Abstract

Purpose: Neuronal cell loss and accumulation of extracellular deposits in the brain are features of Alzheimer’s disease (AD). Thinning of the retinal nerve fibre layer (RNFL) and increased accumulation of drusen had been proposed to occur in the eye in AD. It is, however, not clear whether these abnormalities in the eye are specific for AD. Here we report on the preliminary results of two studies examining this association.

Methods: Colour and autofluoresecnce (OPTOMAP P200C AF) images of healthy controls (HC) and patients with typical AD were taken. Study two: Optical coherence tomography (OPTOS OCT LSO) of HC, AD and posterior cortical atrophy (PCA; predominant impairments in visual perception and other posterior cortical functions) were collected. The study had full local Ethical Committee approval. Overall we examined 81 controls, 13 PCA and 70 AD patients. Images were analysed for presence/absence and progression of drusen or RNFL thickness and macular retinal volume. Statistical analysis was carried out using STATA and SPSS.

Results: Study one: There was no significant age difference between AD and HC (77.7±7.2 vs. 71.3±10.2; p>0.1) (AD MMSE scores were <26). Drusen in both AD and HC progressed in two years. However, progression in AD was more prevalent in all zones (Zone1-3: 19.2% vs 3.3%; Zone 4: 17.2% vs 8.3% ; Zone 5: 12.0% vs 4.2%). Study Two: There were no significant age differences between HC, AD and PCA (65.0±8.8, 63.3±7.0 and 64.8±6.0, respectively). MMSE scores were HC>29, AD< 21 and PCA<23. RNFL were thinned in both AD and PCA compared to HC especially in the superior and inferior quadrants. The overall volume of the macula in AD and PCA was lower than in HC.

Conclusions: These results confirmed that both drusen deposition and changes in RNFL and overall volume of the macula appears to be affected by the pathological event leading to AD. Data from more participants, from follow up studies and information from brain imaging of the same participants will help to clarify whether events in the eye might be used as surrogate markers for brain pathologies.

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