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Invited Review

Reticular pseudodrusen: current understanding

, MD BSc & , MBBS PhD FRANZCO FAAHMS
Pages 455-462 | Received 15 Apr 2018, Accepted 28 Aug 2018, Published online: 15 Apr 2021
 

Abstract

Reticular pseudodrusen (RPD), also known as subretinal drusenoid deposits, represent a morphological change to the retina distinct from other subtypes of drusen by being located above the level of the retinal pigment epithelium. Although they can infrequently appear in individuals with no other apparent pathology, their highest rates of occurrence are in association with age‐related macular degeneration (AMD), for which they hold clinical significance by being highly correlated with end‐stage disease sub‐types, choroidal neovascularisation and geographic atrophy. Reticular pseudodrusen are also found in other diseases, most notably Sorsby's fundus dystrophy, pseudoxanthoma elasticum and acquired vitelliform lesions. They are found more frequently in females, with increased age and more commonly bilaterally than unilaterally. Increased risk of RPD formation is conveyed by genetic variants known to increase risk of AMD development, including complement factor H, age‐related maculopathy susceptibility 2, and high‐temperature requirement A serine peptidase 1; however, to date, no genetic factor has been found to predispose to RPD independent of those that carry risks for AMD. They have typical features visible on multimodal imaging, identifiable either as single lesions or more commonly in yellowish‐white net‐like patterns on colour fundus photography and are particularly distinguishable using spectral domain optical coherence tomography, fundus auto‐fluorescence, and near infrared reflectance imaging. On histological examination, RPD have been shown to have distinct compositions in comparison to typical drusen, suggesting different pathways of pathogenesis. Although their aetiology remains unclear, presence of opsin within lesions, a high topographic association with areas of highest rod‐photoreceptor concentration and functional deficits most pronounced within the scotopic range, has implicated rod photoreceptor dysfunction as a component of RPD.

ACKNOWLEDGEMENTS

Supported by National Health and Medical Research Council (NHMRC) Fellowship (#1103013, RHG). The Centre for Eye Research Australia (CERA) receives Operational Infrastructure Support from the Victorian Government, Australia.

Additional information

Funding

National Health and Medical Research Council (NHMRC)
The Centre for Eye Research Australia (CERA)
Victorian Government, Australia

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