INVESTIGADORES
DORFMAN Damian
congresos y reuniones científicas
Título:
Melatonin protects the retinal pigmentary epithelium and photoreceptor damage within experimental nonexudative age related macular denegeration
Autor/es:
HERNÁN DIÉGUEZ; HORACIO E ROMEO; AGUSTINA ALAIMO; MARÍA FLORENCIA GONZÁLEZ FLEITAS; RUTH E. ROSENSTEIN; DAMIÁN DORFMAN
Reunión:
Congreso; XXXIV Reunión Anual de la SAN; 2019
Resumen:
Non-exudative age-related macular degeneration (NE-AMD), the main cause of blindness inthe elderly, is characterized by retinal pigment epithelium (RPE) and photoreceptors (PR) atrophy exclusively circumscribed tothe macula. There are no effective therapeutic strategies that can prevent or delay the NE-AMD. It has been suggested that RPEoxidative damage plays an important role in NE-AMD pathogenesis. Melatonin is an effective antioxidant and has proven effects within several retinal neurodegenerative disorders. We have developed a NE-AMD model induced by superior cervicalganglionectomy (SCGx) in adult C57BL/6J mice, which reproduces NE-AMD hallmarks exclusively circumscribed to the central temporal RPE/outer retina, a region comparable to the human macula. In this context, the aim of this work was analyzing the effect of melatonin on thealterations induced by SCGx. Melatonin prevented the visual function, the decrease in RPE melanin content and RPE65-inmunorreactivity, and the RPE and PR ultrastructural alterations at 10 weeks post-SCGx. Moreover, melatonin prevented the decrease in mitochondrial mass (MitoTrackerRed (+) area, and levels of specific mitochondrial proteins) as well as the increase in RPE and PR oxidative stress markers at 6 weeks post-SCGx. These findings suggest that melatonin could be a possible novel therapy for treat thedAMD.