Retina World Congress 2026: The dopamine-AMD connection

The relationship between dopamine signaling and age-related macular degeneration (AMD) is an emerging area of interest that could have practical implications for how clinicians think about the medications their patients are already taking. That was the message from Sharon Fekrat, MD, FACS, FASRS, vice chair of faculty affairs and Robert Machemer Distinguished Professor of Ophthalmology at Duke University School of Medicine and retina specialist at Duke Health, who addressed the topic at Retina World Congress 2026, May 14 to 17, in Fort Lauderdale, Florida.

Fekrat explained the biological rationale for the dopamine-AMD connection. When light enters the eye and reaches the retina, dopamine is released by amacrine cells. As patients age, that dopamine release decreases, providing a potential mechanism for some of the changes seen in eyes with AMD. She noted that dopamine receptors are present not only in the retina but also in the retinal pigment epithelium.

Current evidence and clinical implications

Fekrat noted that the field is not yet at a stage where dopaminergic therapies should change clinical practice. "It's not ready at this juncture in order to change the way that we practice," she said. She added that there have been no clinical trials or multicenter trials looking at dopaminergic therapies in AMD, and that the current evidence base consists of animal work and retrospective database analyses, including work from her group at Duke and a group at Northwestern.

She identified 2 categories of dopaminergic agents with potentially opposing effects in AMD. Dopamine precursors and agonists such as levodopa, used in patients with Parkinson disease, may decrease progression to geographic atrophy (GA). Dopamine antagonists, including haloperidol, metoclopramide, and risperidone, may increase the chance of progression to wet AMD. Fekrat suggested that clinicians begin paying closer attention to the oral medications their patients are taking in light of these signals, while stopping well short of recommending that patients discontinue medications such as antipsychotics at this stage.

She placed dopaminergic therapies within the broader AMD treatment landscape, noting that dopamine would most likely be used earlier in the treatment paradigm—in early or intermediate AMD—as a strategy to decrease progression to GA. She also referenced other emerging prevention-focused approaches including photobiomodulation in intermediate AMD and the anticipated AREDS3 data.

On the path forward, Fekrat noted that an industry-sponsored clinical trial is unlikely given that these are already available medications, and suggested that post hoc analyses of already completed trials could be a viable avenue for generating additional evidence. In the meantime, she encouraged clinicians to note when patients with AMD are taking levodopa, which may be protective against progression to GA, or dopamine antagonists, which may help explain why some patients with choroidal neovascularization are harder to treat and may not respond as well as expected to existing pharmacotherapy.