Abstract
Retinitis Pigmentosa (RP) is a genetically heterogeneous disease that affects 1 in 3500 people globally (Pagon, 1988). Regardless of the causative mutation, the endpoint is the same; photoreceptor cell death occurs via apoptosis. The mechanisms that cause program cell death (PCD) in photoreceptors remain elusive. Anti-apoptotic strategies have shown promise as a therapeutic approach in the treatment of neurodegenerative diseases in animal models. Since the retina is of neuronal origin, it may be possible to treat RP by blocking the apoptotic cascade in photoreceptors, irrespective of the mutation involved, thereby delaying, if not preventing altogether, progression of the disease.
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Petrin, D. et al. (2003). XIAP Protects Photoreceptors from N-Methyl-N-Nitrosourea-Induced Retinal Degeneration. In: LaVail, M.M., Hollyfield, J.G., Anderson, R.E. (eds) Retinal Degenerations. Advances in Experimental Medicine and Biology, vol 533. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0067-4_49
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DOI: https://doi.org/10.1007/978-1-4615-0067-4_49
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