Age-related macular degeneration
● Symptoms and Causes
Age-related macular degeneration affects photoreceptors, the retinal pigment epithelium, the Bruch membrane, and the choriocapillaris (the innermost layer of the choroid) in the macula, the central portion of the retina responsible for sharp vision. AMD is a multifactorial disease related to aging, genetic susceptibility, and environmental risk factors. Aging-related changes include increasing resistance, rarefication, and loss of choriocapillaris, lipid and lipoprotein deposition in the Bruch membrane, and reduction in photoreceptor density. In AMD, these changes, coupled with chronic inflammation, altered lipid and lipoprotein deposition, increased oxidative stress, and impaired extracellular matrix maintenance, lead to formation of extracellular deposits containing lipids, minerals, or proteins, namely drusen, the hallmark lesions of early and intermediate AMD. Progression of AMD is characterized by advancing photoreceptor and retinal pigment epithelium degeneration, which includes migration of retinal pigment epithelium cells from their original attachment at the Bruch membrane into the more inner layers of the retina . Genetic susceptibility plays a substantial role in the etiology of AMD. Genome-wide association studies reported genes involved in biological pathways that include inflammation and immunity, lipid metabolism and transport, cellular stress and toxicity, and extracellular matrix maintenance, respectively, to be associated with AMD,7 with 2 major loci, CFH8-11 and ARMS2-HTRA1.Cigarette smoke is the most consistently reported environmental risk factor for AMD.
JAMA.2024;331(2):147-157.doi:10.1001/jama.2023.26074
Age-related macular degeneration
● Symptoms and Causes
Age-related macular degeneration affects photoreceptors, the retinal pigment epithelium, the Bruch membrane, and the choriocapillaris (the innermost layer of the choroid) in the macula, the central portion of the retina responsible for sharp vision. AMD is a multifactorial disease related to aging, genetic susceptibility, and environmental risk factors. Aging-related changes include increasing resistance, rarefication, and loss of choriocapillaris, lipid and lipoprotein deposition in the Bruch membrane, and reduction in photoreceptor density. In AMD, these changes, coupled with chronic inflammation, altered lipid and lipoprotein deposition, increased oxidative stress, and impaired extracellular matrix maintenance, lead to formation of extracellular deposits containing lipids, minerals, or proteins, namely drusen, the hallmark lesions of early and intermediate AMD. Progression of AMD is characterized by advancing photoreceptor and retinal pigment epithelium degeneration, which includes migration of retinal pigment epithelium cells from their original attachment at the Bruch membrane into the more inner layers of the retina . Genetic susceptibility plays a substantial role in the etiology of AMD. Genome-wide association studies reported genes involved in biological pathways that include inflammation and immunity, lipid metabolism and transport, cellular stress and toxicity, and extracellular matrix maintenance, respectively, to be associated with AMD,7 with 2 major loci, CFH8-11 and ARMS2-HTRA1.Cigarette smoke is the most consistently reported environmental risk factor for AMD.
JAMA.2024;331(2):147-157.doi:10.1001/jama.2023.26074