Investigating the Role of The Antioxidant N-acetylcarnosine in Attenuating Oxidation-induced Retinal Damage in Retinitis Pigmentosa

Abstract

The goal of this research was to explore the strong antioxidant, n-acetylcarnosine, in its capacity to ameliorate oxidative stress, specifically in the context of slowing disease progression of retinal degeneration. Retinal degeneration affects one out of 1000 individuals globally, with 95% of these retinal diseases sparked by a genetic origin. Since the large majority of genetic-based retinal diseases lead to dysfunction and aberration of rod and cone photoreceptor cells, with a byproduct of this disease progression resulting in oxidative stress that further facilitates disease progression, a novel broad-spectrum therapy that targets this common element, rather than specific genes, is necessary (Haider, 2020). This study identified both topical as well as injection-based modalities as potential routes of photoreceptor recovery in the rd1 disease model, with a near-doubling of the surmised inner nuclear layer during the injection-based study, as evidenced by histology images. While additional studies are needed to better identify the nature of the cells rescued, these initial studies paint n-acetylcarnosine as a promising prodrug for photoreceptor rescue and as a novel retinal disease therapeutic.