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Glaucoma, a progressive age-related optic neuropathy characterized by the death of retinal ganglion cells, is the most common neurodegenerative cause of irreversible blindness worldwide. The therapeutic management of glaucoma, which is limited to lowering intraocular pressure, is still a challenge since visual loss progresses in a significant percentage of treated patients. Restricted dietary regimens have received considerable attention as adjuvant strategy for attenuating or delaying the progression of neurodegenerative diseases. Here we discuss the literature exploring the effects of modified eating patterns on retinal aging and resistance to stressor stimuli.

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.