gms | German Medical Science

Background: The pathologic mechanism responsible for the death of RPE, a hallmark of geographic atrophy, is currently unclear.

Methods: Our investigations utilize human donor tissue graded for the presence and severity of AMD using the Minnesota Grading System. The experimental approach is to study changes in cellular composition, mtDNA damage and mitochondrial function in human donors at progressive stages of AMD using a combination of proteomic and molecular biology techniques, as well as performing functional testing on primary RPE cultures.

Results: Results from multiple analyses led to the unique observation that the mitochondria in the RPE are negatively impacted by the disease. Thus, RPE mitochondrial dysfunction may be driving AMD pathology.

Conclusion: Treatments that that preserve or improve mitochondrial function may be an effective therapy for slowing down or stopping vision loss in patients with early AMD.