ENRICHED ENVIRONMENT PROTECTS THE CENTRAL OUTER RETINA AGAINST EXPERIMENTAL NON-EXUDATIVE AGE-RELATED MACULAR DEGENERATION IN MICE

DORFMAN, DAMIÁN; BERNAL AGUIRRE, NATHALY; CALANNI, JUAN S.; ALAIMO, AGUSTINA; ROMEO, HORACIO E.; ROSENSTEIN, RUTH E; DIEGUEZ, HERNÁN H

Mar del Plata

Congreso; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS 2022; 2022

SAIC, SAI, FAIC, SAFIS

423. (405) Non-exudative age-related macular degeneration(NE-AMD), the main cause ofblindness in the elderly, is characterized by retinal pigmentepithelium (RPE) and photoreceptors (PR) atrophy circumscribed to the macular area. There are no effectivetherapies to prevent or delay thevision loss that affects patients with NE-AMD.We have developed a NE-AMD model induced bysuperior cervicalganglionectomy (SCGx) in C57BL/6J mice, which reproduces thedisease hallmarks exclusively circumscribed to the temporal region of the RPE/PR. Environmental enrichment (EE) is a complex combinationof physical and inanimate stimulation, which has proven neuroprotective effects against retinal neurodegeneration.The aim of this work wasanalysing the protective effect of the exposure toEE on the alterations induced by experimental NE-AMD. Adult maleC57BL/6J mice were submitted to unilateral SCGx, whereas thecontralateral side was submitted to a sham procedure. Animals weresubmitted to SCGx and exposed to a standard environment (SE)or EE for 10 weeks. SCGx induced a significant increase in ubiquitouschoroid thickness (p<0.01), a significant decrease in theelectroretinogram a-wave amplitude (p<0.01) and performance invisual behaviour tests (p<0.01), a significant decrease of RPE melanin content and RPE65-immunoreactivity(p<0.01), a significant decrease inmitochondria mass and increase in mitochondria superoxideand lipid peroxidation products (p<0.01), and RPE and PRultrastructural alterations at the temporal region. Although, EE didnot prevent choroid alterations, it completely preserved visual function, and RPE and PR structure (p<0.01).EE preserved mitochondria mass andstructure (p<0.01) and prevented RPE oxidative stress (p<0.01). These results suggest that EEprevented the functional andstructural damage induced by experimental NE-AMD, throughprotecting RPE mitochondria and preventing RPE oxidative damage,thus becoming as a promising therapeutic strategy for NE-AMD.