Age-related macular degeneration (AMD) represents a significant health concern, recognized as a leading cause of central vision loss among older adults. This progressive disease affects the macula, which is the small but specialized central part of the retina responsible for seeing fine details and straight-ahead tasks like reading and driving. The damage to this area causes a blurring or blind spot in the center of the visual field, while peripheral vision usually remains unaffected. Understanding the condition begins with recognizing that AMD is broadly categorized into two primary forms: the dry form and the wet form. The distinction between these two types is based on their underlying biological processes and is important because it dictates the appropriate course of diagnosis and treatment.
Dry Age-Related Macular Degeneration
Dry AMD is the more prevalent form, accounting for 80 to 90 percent of all diagnosed cases. The pathology is characterized by the gradual deterioration and thinning of the light-sensitive tissues in the macula. This involves the slow accumulation of yellowish deposits called drusen, composed of extracellular waste material, beneath the retina. The presence of drusen is often the first clinical sign of AMD, and while small deposits may not cause symptoms, their increase in size and number signals an advancing stage of the disease. Vision loss is typically slow and gradual, occurring over many years as the macula’s cells become damaged, leading to central vision blurring or difficulty seeing in dim light. The advanced stage of dry AMD is known as geographic atrophy (GA), where regions of the retinal pigment epithelium and underlying cells die off. GA results in clearly demarcated patches of vision loss that slowly expand over time.
Wet Age-Related Macular Degeneration
Wet AMD is a less common but generally more severe form of the condition, responsible for the majority of profound vision loss cases. This form is defined by an abnormal biological event called choroidal neovascularization. This is the spontaneous growth of fragile, new blood vessels that originate from the choroid, the layer of blood vessels beneath the retina, and extend under the macula. These newly formed vessels are structurally unsound and prone to leaking blood and fluid into the macula. The presence of fluid or blood causes the macula to swell or lift from its normal position, which rapidly distorts and destroys central vision. This leakage is often stimulated by an overabundance of a protein called Vascular Endothelial Growth Factor (VEGF). Because of the potential for rapid and severe damage, the onset of Wet AMD symptoms, such as the sudden warping of straight lines, is considered a medical urgency requiring immediate evaluation. Progression from dry to wet AMD occurs in about 10 to 15 percent of dry cases.
Contrasting Management and Treatment Approaches
The distinct pathologies of dry and wet AMD necessitate fundamentally different management and treatment strategies. For individuals with dry AMD, especially those in the intermediate stage, there is currently no medical intervention that reverses the existing damage. Management focuses on slowing the disease’s progression and includes regular monitoring through comprehensive eye exams. Lifestyle factors, such as smoking cessation and maintaining a healthy diet rich in dark, leafy greens, are strongly encouraged to support retinal health.
A specific nutritional regimen, based on the Age-Related Eye Disease Study (AREDS and AREDS2) research, is recommended for certain patients to slow the progression to advanced AMD. These AREDS2 supplements contain a precise combination of high-dose antioxidant vitamins (C and E), minerals (zinc and copper), and carotenoids (lutein and zeaxanthin). Taking this supplement daily can reduce the risk of advanced AMD progression, including the development of geographic atrophy, by about 25 percent in those with intermediate disease.
In stark contrast, Wet AMD requires immediate and active medical intervention aimed at stopping the abnormal vessel growth and leakage. The gold standard treatment involves intravitreal injections of anti-VEGF drugs, such as aflibercept, ranibizumab, or bevacizumab. These medications are injected directly into the eye to block the action of the VEGF protein, thereby suppressing the formation of new vessels and reducing the leakage of fluid and blood. Patients typically require a loading phase of injections, followed by a long-term maintenance schedule that is adjusted based on the individual’s response to the drug. While anti-VEGF therapy has revolutionized the prognosis for Wet AMD by often stabilizing or even improving vision, it is not a cure and requires ongoing treatment to maintain its effect. Less common interventions, such as photodynamic therapy or thermal laser procedures, are sometimes used for specific types of neovascularization, but anti-VEGF injections remain the primary and most effective strategy.