PURPOSE: A review regarding the pathophysiology of AMD as shown in the literature RESULTS: Targets in AMD treatment include: 1. Protection against oxidative stress; 2. Prevention of the accumulation of lipofuscin; 3. Reduction or elimination of chronic inflammation; 4. Changes involving the participation of complement inflammatory phenomena; 5. Changes in the phenomena of chronic inflammation which do not involve the participation of complement (eg. Mitochondria and extracellular matrix). The Neovascularization process includes: 1. Production of angiogenic factor; 2. Release of angiogenic factor; 3. The binding of factors to extracellular receptors and activation of intracellular signaling; 4. Activation of endothelial cells with basement membrane degradation; 5. Endothelial cell proliferation; 6. Endothelial cell migration; 7. Remodeling of extracellular matrix; 8. Tube formation; 9. Vascular stabilization. CONCLUSIONS: Therapy inAMD, based on physiological characteristics of early and late stages, is possible nowadays. It is possible to apply a specific treatment for each stage of AMD, but effective treatment requires combinations of specific therapeutic remedies involving different pathophysiological pathways.
PURPOSE: A review regarding the pathophysiology of AMD as shown in the literature RESULTS: Targets in AMD treatment include: 1. Protection against oxidative stress; 2. Prevention of the accumulation of lipofuscin; 3. Reduction or elimination of chronic inflammation; 4. Changes involving the participation of complement inflammatory phenomena; 5. Changes in the phenomena of chronic inflammation which do not involve the participation of complement (eg. Mitochondria and extracellular matrix). The Neovascularization process includes: 1. Production of angiogenic factor; 2. Release of angiogenic factor; 3. The binding of factors to extracellular receptors and activation of intracellular signaling; 4. Activation of endothelial cells with basement membrane degradation; 5. Endothelial cell proliferation; 6. Endothelial cell migration; 7. Remodeling of extracellular matrix; 8. Tube formation; 9. Vascular stabilization. CONCLUSIONS: Therapy inAMD, based on physiological characteristics of early and late stages, is possible nowadays. It is possible to apply a specific treatment for each stage of AMD, but effective treatment requires combinations of specific therapeutic remedies involving different pathophysiological pathways.