Photoreceptor Layer Topography in Children with Leber Congenital Amaurosis Caused byRPE65Mutations
Investigative Ophthalmology & Visual Science2008Vol. 49(10), pp. 4573–4573
Citations Over TimeTop 10% of 2008 papers
Samuel G. Jacobson, Artur V. Cideciyan, Tomás S. Alemán, Alexander Sumaroka, Elizabeth A. M. Windsor, Sharon Schwartz, Elise Héon, Edwin M. Stone
Abstract
Photoreceptor loss in the foveal and extrafoveal retina was prominent, even in the youngest patients studied. Differences in the topography of residual photoreceptors in children with RPE65-LCA suggest that it may be advisable to use individualized ONL mapping to guide the location of subretinal injections for gene therapy and thereby maximize the potential for efficacy.
Related Papers
- → Rpe65 Is the Retinoid Isomerase in Bovine Retinal Pigment Epithelium(2005)424 cited
- → Leber congenital amaurosis due to RPE65 mutations and its treatment with gene therapy(2010)248 cited
- → Retinal pigment epithelium 65 kDa protein (RPE65): An update(2021)85 cited
- → Lentiviral Gene Transfer of Rpe65 Rescues Survival and Function of Cones in a Mouse Model of Leber Congenital Amaurosis(2006)116 cited
- → Evidence for RPE65‐independent vision in the cone‐dominated zebrafish retina(2007)54 cited