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Age-related macular degeneration (AMD) is the primary cause of blindness among the elderly worldwide. To date, no cure is available, and the available palliative treatments only showed limited efficacy in improving visual acuity. The etiology of AMD remains elusive but research over the past decade has uncovered characteristic features of the disease.
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Known as the hallmarks of AMD, these features include (A) oxidative stress and RPE cytotoxicity; (B) loss of macromolecular permeability and hydraulic conductivity: (C) inflammation; (D) choroidal neovascularization and vascular leakage; and (E) loss of neuroprotection. Recent breakthrough in understanding the pathogenesis of AMD has spawned an array of novel therapeutic agents designed to address these hallmarks. Here we review the features of AMD and highlight the most promising therapeutic and diagnostic approaches based on the patents published from 2008 to 2011. Most likely, a next generation treatment for AMD will be developed from these emerging efforts. Introduction Age-related macular degeneration (AMD) is the primary cause of blindness among people over 50 years old ().
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Globally, 33 million individuals are affected by AMD with the direct cost estimated at $255 billion (). In the United States alone, 1.8 million individuals are afflicted by AMD and the number is estimated to increase to an epidemic level of almost 3 million by 2020 (). Early AMD is characterized by drusen (yellow spots) and hypopigmention or hyperpigmentation in the choroid/retinal pigment epithelium (RPE) layers in the macula (–). Late AMD has interconvertible “dry” and “wet” forms. The advanced form of dry AMD, also called geographic atrophy (GA), is characterized by extensive loss of the RPE, as well as its neighboring photoreceptors (PR) and choriocapillaris.
Choroidal neovascularization (CNV), which involves abnormal growth of blood vessels from the choroid into the retina, is a hallmark of wet (or neovascular) AMD. Although, its etiology remains unknown, AMD is suggested to be a multifactorial disease. A mixture of sustained oxidative stress, chronic inflammation and genetic predispositions appear to alter the architecture and the health of the retina, which ultimately leads to dry and wet AMD. To date, no cure is available for dry AMD, and the palliative treatments for wet AMD are restricted to anti-neovascularization agents, photodynamic therapy and thermal laser (). Encouragingly, there has been a fivefold increase in the number of patents for therapeutic agents targeting the disease hallmarks over the past decade (). The current review highlights the recent patents describing novel therapeutic approaches to address the hallmarks of AMD.
Hallmarks of AMD and their genetic basis Recent genome-wide association studies (GWAS) together with cell culture or animal models are starting to unravel the genetic and pathogenic mechanisms of AMD. These extensive studies have suggested that the following hallmarks tend to drive the disease progression, which include: (A) oxidative stress and RPE cytotoxicity; (B) loss of macromolecular permeability and hydraulic conductivity: (C) inflammation; (D) choroidal neovascularization and vascular leakage; and (E) loss of neuroprotection. Accordingly, numerous patents aiming at controlling these critical processes using novel therapeutic approaches have been filed in recent years. (A) Oxidative stress and RPE cytotoxicity Oxidative stress is a critical component in the pathogenesis of AMD. Cigarette smoking, which poses systemic oxidative stress, has been shown to be a significant risk factor for AMD ().
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