Deletion of M-opsin Prevents “M cone” Degeneration in a Mouse Model of Leber Congenital Amaurosis

April 28, 2020 | Histopathology

Fresh from The American Journal of Pathology, here is a new Histopathology article for you:

Mutations in RPE65 or lecithin-retinol acyltransferase (LRAT) disrupt 11-cis-retinal synthesis and cause Leber congenital amaurosis (LCA). Despite the success of recent RPE65 gene therapy, follow-up studies show that patients continue to experience photoreceptor degeneration and lose vision benefit over time. In Lrat–/– mouse model, mislocalized medium (M)-wavelength opsin was degraded, whereas mislocalized short (S)-wavelength opsin accumulated before the onset of cone degeneration. The mechanism for the foveal medium (M)/long (L)-wavelength cone photoreceptor degeneration in LCA is unknown.... Read more at  The American Journal of Pathology Blog.

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