Affiliation:
1. Nuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, Oxford University, Oxford OX3 9DU, UK
2. Oxford Eye Hospital, Oxford University NHS Foundation Trust, Oxford OX3 9DU, UK
Abstract
Age-related macular degeneration (AMD) is the leading cause of vision loss and visual impairment in people over 50 years of age. In the current therapeutic landscape, intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapies have been central to the management of neovascular AMD (also known as wet AMD), whereas treatments for geographic atrophy have lagged behind. Several therapeutic approaches are being developed for geographic atrophy with the goal of either slowing down disease progression or reversing sight loss. Such strategies target the inflammatory pathways, complement cascade, visual cycle or neuroprotective mechanisms to slow down the degeneration. In addition, retinal implants have been tried for vision restoration and stem cell therapies for potentially a dual purpose of slowing down the degeneration and restoring visual function. In particular, therapies focusing on the complement pathway have shown promising results with the FDA approved pegcetacoplan, a complement C3 inhibitor, and avacincaptad pegol, a complement C5 inhibitor. In this review, we discuss the mechanisms of inflammation in AMD and outline the therapeutic landscapes of atrophy AMD. Improved understanding of the various pathway components and their interplay in this complex neuroinflammatory degeneration will guide the development of current and future therapeutic options, such as optogenetic therapy.
Funder
National Institute for Health and Care Research-Oxford Biomedical Research Centre
Medical Research Council
Wellcome Trust
Macular Society Seedcorn Grant
University of Oxford Clarendon-Keble de Breyne and Ramsay Scholarship
University of Oxford Clarendon Fund and Merton College Tira Wannamethee Graduate Scholarship
Cited by
3 articles.
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