The role of inflammation and neurodegeneration in diabetic macular edema

Abstract

The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.

Keywords: diabetic macular edema; inflammation; neurodegeneration.

Figure 1.

(a) Fundus autofluorescence of the right eye of a 71-year-old diabetic man with diabetic macular edema (DME) demonstrating areas of increased foveal autofluorescence where DME cysts are located, (b) infrared retinal image of the same eye, and (c) spectral domain optical coherence tomography encompassing the fovea (horizontal section) showing a subfoveal neuroretinal detachment and multiple hyperreflective retinal spots throughout all retinal layers, especially in the outer retina.