Melatonin protects the retinal pigmentary epithelium and photoreceptor damage within experimental nonexudative age related macular denegeration

HERNÁN DIÉGUEZ; HORACIO E ROMEO; AGUSTINA ALAIMO; MARÍA FLORENCIA GONZÁLEZ FLEITAS; RUTH E. ROSENSTEIN; DAMIÁN DORFMAN

Congreso; XXXIV Reunión Anual de la SAN; 2019

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.