Age-related macular degeneration (AMD) is a neurodegenerative disorder characterized by photoreceptor and retinal pigment epithelium loss often complicated by neovascularization and is one of the leading causes of irreversible vision loss worldwide. However, the precise pathophysiology of AMD remains to date unclear, and there is a dearth of effective therapies for the early stages of the disease. A growing body of evidence has identified microglia-mediated neuroinflammation as a key driver of neuronal damage in AMD, presenting a novel avenue for the development of pharmacological agents targeting this cell population. The local microglial response interacts with other glia as well as engages in crosstalk with peripheral immunological niches. This article presents a review of the current evidence regarding the involvement of glia in the pathophysiology of AMD, an overview of the key immune circuits and effector mechanisms shown to be active in AMD, and potential therapeutic avenues targeting glial involvement.
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