Neuroinflammation as a target for glaucoma therapy

Abstract

The pathogenesis of glaucoma is still not fully clarified but a growing body of evidence suggests that neuroinflammation and immune response are part of the sequence of pathological events leading to the optic neuropathy. Indeed, inflammation - involving the activation and proliferation of resident glial cells (astrocytes, Muller cells and microglia) and the release of a plethora of anti- and pro-inflammatory cytokines, chemokines and reactive oxygen species - has been reported as common features in clinical and experimental glaucoma. In the insulted retina, as for other neuronal tissues, pathogenic and reparative aspects coexist in the inflammatory process, with extent and persistency affecting the final outcome. In view of this, therapies aimed at modulating the immune and inflammatory responses may represent a promising approach for limiting the optic nerve damage and the loss of retinal ganglion cells associated with glaucoma.

Keywords: glaucoma; immune response; inflammasome; microglia; neurodegeneration; neuroinflammation; oxidative stress; retinal ganglion cells.

Figure 1

Neuroinflammation and oxidative stress lead to retinal ganglion cell (RGC) neurodegeneration. CoQ10: Coenzyme Q10; NO: nitric oxide; ROS: reactive oxygen species; AGEs: advanced glycation end products; TNF-α: tumor necrosis factor-alpha; IL-1β: interleukin-1β; IL-6: interleukin-6.