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Chapter-12 Can Antioxidants Rescue Photoreceptors in Retinitis Pigmentosa?

BOOK TITLE: Nutrition and the Eye

Author
1. Pinelli Roberto
2. Elborgy Ebrahim
ISBN
9788184488623
DOI
10.5005/jp/books/11052_12
Edition
1/e
Publishing Year
2010
Pages
3
Author Affiliations
1. Istituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, 70, 25124 Brescia, Italy, Istituto Laser Microchirurgia Oculare Crystal Palace, Via Cefalonia 70 25124, Brescia, Italy, European School for Advanced Studies in Ophthalmology (ESASO), Universitá della Svizzera Italiana, Lugano, Switzerland, Microchirurgia Oculare, Crystal Palace, Suite, Via Cefalonia, 70 25124 Brescia - Italy, Istituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, 70, Brescia, Italy, Istituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, Brescia, Italy, www.ilmo.it, Istituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, Brescia, Italy, Instituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, Brescia, Italy, Istituto Laser Microchirurgia Oculare, Crystal Palace, Via Cefalonia, 70, 25124, Brescia, Italy, Istituto Laser Microchirurgia, Oculare Crystal Palace, Via Cefalonia, 70, 25124, Brescia, Italy, Crystal Palace Via Cefalonia, 70 25124 Brescia, Italy, Istituto Laser
2. Research Institute of Ophthalmology, Giza, Egypt
Chapter keywords

Abstract

Retinitis pigmentosa (RP) is a prevalent cause of blindness caused by a large number of different mutations in many different genes. The mutations result in rod photoreceptor cell death, but it is unknown why cones die. In 2005, a study tested the hypothesis that cones die from oxidative damage by performing immunohistochemical staining for biomarkers of oxidative damage in a transgenic pig model of RP. The demonstration that oxidative damage contributes to cone cell death in RP has important clinical implications. It provides a therapeutic target that may apply to all RP patients. The enormous genetic heterogeneity among the diseases that constitute RP is a problem for the development of treatments that deal whit primary genetic defects; any such treatments will apply to a very small fraction of patients whit RP. Treatments involving neurotrophic factors also have broad applicability and are important to pursue. It is likely that benefits will be additive or synergistic by reducing oxidative damage to cones while simultaneously increasing the threshold for apoptosis with neurotrophic factors.

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