Abstract
Age-related macular degeneration (AMD) is a complex multifactorial disease characterized in its late form by neovascularization (wet type) or geographic atrophy of the retinal pigment epithelium cell layer (dry type). The complement system is an intrinsic component of innate immunity. There has been growing evidence that the complement system plays an integral role in maintaining immune surveillance and homeostasis in AMD. Based on the association between the genotypes of complement variants and AMD occurrence and the presence of complement in drusen from AMD patients, the complement system has become a therapeutic target for AMD. However, the mechanism of complement disease propagation in AMD has not been fully understood. This concise review focuses on an overall understanding of the role of the complement system in AMD and its ongoing clinical trials. It provides further insights into a strategy for the treatment of AMD targeting the complement system.
Highlights
Age-related macular degeneration (AMD) is a leading cause of vision loss in elderly people in developed countries [1,2,3]
The Age-related Eye Disease Study (AREDS) research group classified paSimplified classification scales according to the clinical features for AMD have been tients into four categories according to the size and extent of drusen, presence of geodeveloped
The Age-related Eye Disease Study (AREDS) research group classified patients into four categories according to the size and extent of drusen, presence of geographic atrophy (GA), and neovascular changes [12,13]
Summary
Age-related macular degeneration (AMD) is a leading cause of vision loss in elderly people in developed countries [1,2,3]. It is related to various risk factors and genetic predispositions for a number of patients [4]. Irreversible central vision loss has devastating effects on the physical, social, and emotional aspects of the patients and leads to a high societal cost burden. The treatment options targeting vascular leakage are available only for patients with the neovascular form of the disease. The most important aspects are modifiable risk factors and routine ophthalmic monitoring. This limitation of effective therapeutic options is likely due to incomplete knowledge of the mechanisms involved in AMD pathogenesis.
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