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Natural history of cone disease in the murine model of Leber congenital amaurosis due to CEP290 mutation: determining the timing and expectation of therapy
Journal article   Open access   Peer reviewed

Natural history of cone disease in the murine model of Leber congenital amaurosis due to CEP290 mutation: determining the timing and expectation of therapy

Shannon E Boye, Wei-Chieh Huang, Alejandro J Roman, Alexander Sumaroka, Sanford L Boye, Renee C Ryals, Melani B Olivares, Qing Ruan, Budd A Tucker, Edwin M Stone, …
PloS one, Vol.9(3), pp.e92928-e92928
2014
DOI: 10.1371/journal.pone.0092928
PMCID: PMC3966841
PMID: 24671090
url
https://doi.org/10.1371/journal.pone.0092928View
Published (Version of record) Open Access

Abstract

Mutations in the CEP290 (cilia-centrosomal protein 290 kDa) gene in Leber congenital amaurosis (LCA) cause early onset visual loss but retained cone photoreceptors in the fovea, which is the potential therapeutic target. A cone-only mouse model carrying a Cep290 gene mutation, rd16;Nrl-/-, was engineered to mimic the human disease. In the current study, we determined the natural history of retinal structure and function in this murine model to permit design of pre-clinical proof-of-concept studies and allow progress to be made toward human therapy. Analyses of retinal structure and visual function in CEP290-LCA patients were also performed for comparison with the results in the model. Rd16;Nrl-/- mice were studied in the first 90 days of life with optical coherence tomography (OCT), electroretinography (ERG), retinal histopathology and immunocytochemistry. Structure and function data from a cohort of patients with CEP290-LCA (n = 15; ages 7-48) were compared with those of the model. CEP290-LCA patients retain a central island of photoreceptors with normal thickness at the fovea (despite severe visual loss); the extent of this island declined slowly with age. The rd16;Nrl-/- model also showed a relatively slow photoreceptor layer decline in thickness with ∼80% remaining at 3 months. The number of pseudorosettes also became reduced. By comparison to single mutant Nrl-/- mice, UV- and M-cone ERGs of rd16;Nrl-/- were at least 1 log unit reduced at 1 month of age and declined further over the 3 months of monitoring. Expression of GNAT2 and S-opsin also decreased with age. The natural history of early loss of photoreceptor function with retained cone cell nuclei is common to both CEP290-LCA patients and the rd16;Nrl-/- murine model. Pre-clinical proof-of-concept studies for uniocular therapies would seem most appropriate to begin with intervention at P35-40 and re-study after one month by assaying interocular difference in the UV-cone ERG.
Antigens, Neoplasm - genetics Age Factors Leber Congenital Amaurosis - physiopathology Tomography, Optical Coherence Humans Mice, Inbred C57BL Middle Aged Mice, Transgenic Leber Congenital Amaurosis - genetics Mutation - genetics Disease Progression Animals Light Signal Transduction Time Factors Retinal Cone Photoreceptor Cells - pathology Adolescent Adult Female Neoplasm Proteins - genetics Nuclear Proteins - genetics Child Leber Congenital Amaurosis - therapy Retina - pathology Disease Models, Animal

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