Abstract

Acquired neuro-retinal diseases encompass a spectrum of conditions affecting the neural and retinal structures, leading to vision impairment and, in severe cases, blindness. Recent research has highlighted the potential role of amino acid and sphingolipid metabolism in the pathogenesis of these diseases. This review provides an overview of the differences in amino acid and sphingolipid metabolism observed in patients with acquired neuro-retinal diseases, including age-related macular degeneration, diabetic retinopathy, and retinitis pigmentosa.

Studies have demonstrated alterations in the levels of specific amino acids, such as glutamate, glycine, and taurine, in the vitreous humor and retinal tissues of patients with neuro-retinal diseases, suggesting dysregulation of neurotransmitter balance and excitotoxicity. Additionally, disturbances in sphingolipid metabolism, including changes in ceramide and sphingosine-1-phosphate levels, have been implicated in retinal cell apoptosis, inflammation, and vascular dysfunction. Understanding the metabolic alterations associated with acquired neuro-retinal diseases may provide insights into disease mechanisms and identify potential biomarkers for early diagnosis and monitoring. Furthermore, targeting amino acid and sphingolipid metabolism pathways may offer novel therapeutic strategies for the treatment of these debilitating conditions. This review highlights the importance of metabolic dysregulation in acquired neuro-retinal diseases and its potential implications for disease management and intervention.