Abstract: Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy or retinitis pigmentosa are the most frequent causes of incurable low vision and blindness worldwide. It had been estimated that the prevalence of these diseases varies between 1/750 and 1/5000 depending on the region, the level of consanguinity or ethnicity (Na et al., 2017). The functional and structural complexity of the retina makes it susceptible to multiple types of pathogenic damage. The retinal neurodegeneration may be caused by genetic defects, increased intraocular pressure, high levels of blood glucose or other types of stress or aging. All of them cause progressive neuronal death which is accompanied by a response of glial cells. Although the etiology, pathogenesis and clinical characteristics of retinal neurodegenerative diseases are very different, they have common features because the cellular and molecular response to retinal neurodegeneration is closely similar (Cuenca et al., 2014). Thus, it had been proposed that several neuroprotective therapeutic approaches may be adequate for the retinal neurodegenerative process. Retinal neurodegeneration is characterized by an inflammatory response, oxidative stress and activation of cell death pathways (Cuenca et al., 2014). Besides, the neurodegenerative process of the retina is commonly divided into four different phases and changes that occur during the retina degeneration can be associated with the stage of neurodegeneration (Vugler, 2010; Cuenca et al., 2014; Gagliardi et al., 2019). During phase 1 the function and morphology of the retina appear normal but cell stress induces molecular changes and eventual cell death. In phase 2, cellular stress and the activation of apoptotic pathways leads to progressive cell loss and activation of glial cells. In phase 3, it could be observed a large-scale neuronal cell death which leads glial cells hypertrophy and microglial activation. Phase 4 is characterized by the global retinal alteration with the neuronal cell death, hypertrophy of glial cells, epiretinal membrane formation, invasion by blood vessels and by the migration of the retinal pigment epithelium cells (Cuenca et al., 2014).