New Insights Into EMAP and Its Relationship to AMD

Clinical Report: Rethinking EMAP and Its Relationship to AMD

Overview

At the 2026 SARyV meeting, Alessandro Feo, MD, discussed whether extensive macular atrophy with pseudodrusen-like appearance (EMAP) may be a subtype of late atrophic age-related macular degeneration (AMD), rather than a distinct macular dystrophy. He noted shared features with AMD and diffuse-trickling geographic atrophy (GA), and proposed reevaluating prior GA trial populations because some participants with diffuse-trickling atrophy may have had EMAP.

Background

EMAP was first described in 2009 as a potentially distinct macular dystrophy. The source describes vertical macular atrophy, pseudodrusen-like deposits, and negative genetic testing as characteristic features. Reports have since come from Europe and, increasingly, South America, Asia, and the United States. Its classification matters in the context of GA trials evaluating anticomplement therapies, because the source notes evidence implicating complement in EMAP pathogenesis and similarities to diffuse-trickling GA.

Data Highlights

Topic	Source-reported detail
Initial description	EMAP was described in 2009 by a French group as a potentially distinct macular dystrophy.
Reported features	Vertical macular atrophy, pseudodrusen-like deposits, and negative genetic testing.
Geographic reporting	Reports have expanded from Europe to South America, Asia, and the United States.
Potential AMD relationship	Feo cited presumed basal laminar deposits, a feature shared with AMD, and similarities to diffuse-trickling GA.
Trial relevance	The speakers raised the possibility that some patients classified as having diffuse-trickling GA in prior trials may have had EMAP; no trial reanalysis or numerical treatment results were provided in the article.

Key Findings

EMAP was initially proposed as a separate disease or potentially distinct macular dystrophy when described in 2009.
The source identifies vertical macular atrophy, pseudodrusen-like deposits, and negative genetic testing as characteristic features.
Feo reported that EMAP descriptions now include cases from outside Europe, including South America, Japan, and the United States.
Feo suggested EMAP may represent a variant or subtype of late atrophic AMD, citing presumed basal laminar deposits as a feature shared with AMD.
The source reports evidence that complement is implicated in EMAP pathogenesis and notes similarities between EMAP and the diffuse-trickling GA pattern described by Holz and colleagues.
Feo proposed reevaluating trials that included diffuse-trickling GA because a subset of those patients may have had EMAP; the interview does not report a reanalysis or establish an effect on trial outcomes.

Clinical Implications

The speakers raised the possibility that identifying EMAP among patients enrolled in GA trials could affect interpretation of results from trials of complement-inhibiting therapies. The source does not provide a diagnostic protocol, treatment recommendation, or evidence that reclassification would change clinical outcomes.

Conclusion

The interview presents EMAP as a phenotype whose relationship to late atrophic AMD remains under discussion. Feo called for reevaluation of prior GA trial populations in light of possible overlap with EMAP.