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Emerging treatments for dry age-related macular degeneration (AMD) and geogra phic atrophy focus on two strategies that target components involved in physiopathologi cal pathways: prevention of photoreceptors and retinal pigment epithe lium loss (neuro protection induction, oxidative damage prevention, and visual cycle mo dification) and suppression of inflammation. Neuroprotective drugs, such as ci liary neurotrophic factor, brimonidine tartrate, tandospirone, and anti-amyloid β antibodies, aim to prevent apoptosis of retinal cells. Oxidative stress and depletion of essential micronutrients are targeted by the Age-Related Eye Disease Study (AREDS) formulation. Visual cycle modulators reduce the activity of the photoreceptors and retinal accumulation of toxic fluorophores and lipofuscin. Eyes with dry age-related macular degeneration pre sent chronic inflammation and potential treatments include corticosteroid and com plement inhibition. We review the current concepts and rationale of dry age-rela ted macular degeneration treatment that will most likely include a combination of drugs targeting different pathways involved in the development and progression of age-related macular degeneration.

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Ranibizumab therapy was associated with significant improvements in mean visual acuity and central macular thickness for the group of all patients. Patients who had received bevacizumab treatment within 3 months before initiating ranibizumab treatment had stability of, but no improvement in, visual acuity.

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The association between choroidal osteoma and PCV may have a better prognosis than that with classic CNV. Indocyanine green angiography is a useful tool in characterizing the nature of the neovascularization.

Patients with chronic CSC and a large, dependent serous detachment with peripheral retinal ischemia and neovascularization may be managed by focal treatment to active pigment epithelial leaks alone. This could spare patients of the adverse effects associated with widespread laser treatment and reduce the risk of visual loss due to vitreous hemorrhage and/or more severe complications resulting from progressive retinal ischemia.