Melatonin protects the retina from experimental nonexudative age‐related macular degeneration in mice. Issue 4 (13th March 2020)

• Record Type: Journal Article
• Authors: Diéguez, Hernán H.; González Fleitas, María F.; Aranda, Marcos L.; Calanni, Juan S.; Keller Sarmiento, María I.; Chianelli, Mónica S.; Alaimo, Agustina; Sande, Pablo H.; Romeo, Horacio E.; Rosenstein, Ruth E.; Dorfman, Damián
• Is Part Of: Journal of pineal research. Volume 68:Issue 4(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-03-13
• Subjects: melatonin -- nonexudative age‐related macular degeneration -- oxidative stress -- retinal pigment epithelium -- superior cervical ganglion; Pineal gland -- Periodicals; Pineal Gland -- Periodicals; Épiphyse (Glande); Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 612.492
• DOI: 10.1111/jpi.12643
• Languages: English
• ISSNs: 0742-3098

Abstract

Abstract: Nonexudative age‐related macular degeneration (NE‐AMD) represents the leading cause of blindness in the elderly. Currently, there are no available treatments for NE‐AMD. We have developed a NE‐AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces the disease hallmarks. Several lines of evidence strongly support the involvement of oxidative stress in NE‐AMD‐induced retinal pigment epithelium (RPE) and outer retina damage. Melatonin is a proven and safe antioxidant. Our aim was analysing the effect of melatonin in the RPE/outer retina damage within experimental NE‐AMD. The treatment with melatonin starting 48 h after SCGx, which had no effect on the ubiquitous choriocapillaris widening, protected visual functions and avoided Bruch´s membrane thickening, RPE melanin content, melanosome number loss, retinoid isomerohydrolase (RPE65)‐immunoreactivity decrease, and RPE and hotoreceptor ultrastructural damage induced within experimental NE‐AMD exclusively located at the central temporal (but not nasal) region. Melatonin also prevented the increase in outer retina/RPE oxidative stress markers and a decrease in mitochondrial mass at 6 weeks post‐SCGx. Moreover, when the treatment with melatonin started at 4 weeks post‐SCGx, it restored visual functions and reversed the decrease in RPE melanin content and RPE65‐immunoreactivity. These findings suggest that melatonin could become a promising safe therapeutic strategy for NE‐AMD.