Age-related macular degeneration (AMD) is a progressive eye condition affecting the macula, the central part of the retina responsible for sharp, detailed vision. This damage interferes with the ability to perform tasks like reading, driving, and recognizing faces. AMD is the leading cause of permanent vision loss among older adults in developed nations. There are two primary forms: dry and wet, and the distinction between them is significant because their underlying biology, symptoms, and treatment approaches differ substantially.
Fundamental Differences in Pathology
The two forms of AMD are defined by distinct biological processes occurring beneath the retina. The dry form, which accounts for approximately 80 to 90 percent of all AMD cases, is characterized by the slow deterioration of light-sensing cells in the macula. This process begins with the accumulation of yellowish, fatty deposits known as Drusen, which are composed of lipids and proteins. The presence of Drusen disrupts the normal function of the retinal pigment epithelium (RPE) cells, which nourish the light-sensing cells, leading to their gradual breakdown and eventual vision loss.
The less common wet form, which accounts for about 10 percent of cases, results from a condition called choroidal neovascularization (CNV). In CNV, abnormal, fragile new blood vessels sprout from the choroid, the layer of blood vessels beneath the retina, and push through the RPE cell layer. These new vessels are leaky, releasing fluid and blood into the macula. The leakage and subsequent scarring cause rapid damage to the macula’s structure and function. The progression from dry to wet AMD is often mediated by inflammatory proteins found within the Drusen, which stimulate the release of growth factors that encourage new blood vessel formation.
Distinct Symptoms and Rate of Progression
Dry AMD typically causes a slow, insidious decline in central vision over many years. Early symptoms often include a decrease in the overall clarity of vision, difficulty seeing in dim light, and the need for increasingly brighter illumination for reading. Vision loss from the dry form is usually less severe than the wet form unless it progresses to geographic atrophy, an advanced stage marked by large, clearly defined areas of RPE cell death.
Wet AMD is characterized by a rapid, noticeable onset of vision loss. The leakage of fluid and blood beneath the macula leads to the distinctive symptom of metamorphopsia, where straight lines appear wavy, bent, or distorted. This warping of the visual field is a strong indicator of fluid accumulation and retinal elevation, signaling the rapid progression of the disease. Because wet AMD involves immediate structural damage from leakage, it is responsible for the majority of severe vision loss and legal blindness associated with the condition.
Diagnostic Procedures for Each Type
Diagnosis begins with standard clinical tools, including the Amsler grid, used for at-home monitoring of visual distortion, a common symptom of wet AMD. In the clinic, detailed imaging is performed using Optical Coherence Tomography (OCT), which provides high-resolution cross-sectional images of the retina. OCT effectively visualizes the Drusen deposits characteristic of dry AMD and detects the presence of fluid or swelling beneath the retina, a hallmark of wet AMD.
When wet AMD is suspected, specialized tests are required to locate and map the abnormal blood vessels. Fluorescein Angiography (FA) involves injecting a fluorescent dye into the arm and taking rapid photographs of the retina as the dye travels through the eye’s blood vessels. This test clearly highlights areas of leakage from the fragile new vessels, confirming the diagnosis of CNV. OCT Angiography (OCTA) is a newer, non-invasive alternative that maps the blood flow without requiring dye injection, providing detailed images of the neovascular network.
Targeted Treatment Strategies
The treatment goals and methods for dry and wet AMD are fundamentally different, reflecting their distinct pathologies. For dry AMD, there is currently no intervention that can reverse the damage, so treatment focuses on slowing the rate of progression. This is primarily achieved through lifestyle modifications and specific high-dose nutritional supplements.
The Age-Related Eye Disease Study 2 (AREDS2) formulation has been shown to reduce the risk of advanced AMD progression by about 25 percent in patients with intermediate or advanced disease. The formulation includes:
- Vitamin C
- Vitamin E
- Zinc
- Copper
- Lutein
- Zeaxanthin
Treatment for wet AMD is aggressive and aims to halt the growth and leakage of the abnormal blood vessels. The standard intervention involves the use of anti-vascular endothelial growth factor (anti-VEGF) medications, which are injected directly into the vitreous of the eye. These drugs, including ranibizumab (Lucentis), aflibercept (Eylea), and bevacizumab (Avastin), block the protein that stimulates the growth and leakiness of new blood vessels. Anti-VEGF injections have significantly improved outcomes for wet AMD patients, often stabilizing or even improving vision.