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Muftuoglu, Ilkay Kilic, MD*,†; Ramkumar, Hema L., MD*; Bartsch, Dirk-Uwe, PhD*; Meshi, Amit, MD*; Gaber, Raouf, MD*; Freeman, William R., MD*

doi: 10.1097/IAE.0000000000001759
Original Study

Purpose: To characterize inner retinal damage in patients with dry age-related macular degeneration (AMD) using high-resolution spectral domain optical coherence tomography images.

Methods: Sixty eyes of 60 patients with AMD were categorized using the Age-Related Eye Disease Study (AREDS) severity scale. Spectral domain optical coherence tomography images of these patients were quantified by manually correcting the segmentation of each retinal layer, including the retinal nerve fiber layer, ganglion cell layer, and inner plexiform layer to ensure accurate delineation of layers. The mean ganglion cell complex thickness values (ganglion cell layer + inner plexiform layer + retinal nerve fiber layer) were compared with 30 eyes of 30 healthy subjects.

Results: Ninety percent of eyes (81 eyes) required manual correction of segmentation. Compared with healthy subjects, mean ganglion cell complex thicknesses significantly decreased in more advanced dry AMD eyes, and this decrease was predominantly related to a change in inner plexiform layer thickness. There was no significant difference in thickness-related measurements between milder dry AMD (AREDS-2) eyes and healthy eyes (P > 0.05).

Conclusion: In patients with dry AMD, automatic optical coherence tomography segmentation algorithms may be erroneous. As the severity of dry AMD increases, the inner plexiform layer layer becomes thinned, suggesting that transsynaptic degeneration may be occurring, as the photoreceptor layer is affected by AMD.

In dry age-related macular degeneration, thinning of the ganglion cell complex, mostly due to thinning of the inner plexiform layer, is likely associated with photoreceptor loss and transsynaptic degeneration. This suggests that age-related macular degeneration affects all retinal layers by a mechanism that should be clarified.

*Department of Ophthalmology, Jacobs Retina Center, Shiley Eye Institute, University of California San Diego, La Jolla, California; and

Department of Ophthalmology, Istanbul Training and Research Hospital, Istanbul, Turkey.

Reprint requests: William R. Freeman, MD, University of California San Diego, Jacobs Retina Center, Shiley Eye Institute, 9415 Campus Point Drive, La Jolla, CA 92037; e-mail:

Supported in part by NIH grant R01 EY016323-09A1 (D.-U.B.), a core grant from the National Eye Institute P30 EY022589 (W.R.F.), and an unrestricted grant from Research to Prevent Blindness, NY (W.R.F.). The funding organizations had no role in the design or conduct of this research.

None of the authors has any conflicting interests to disclose.

© 2018 by Ophthalmic Communications Society, Inc.