Age-related Macular Degeneration (AMD) is a progressive eye condition causing central vision loss. The disease targets the macula, a small, specialized area at the center of the retina responsible for sharp, detailed vision needed for tasks like reading and recognizing faces. AMD presents in two fundamentally different forms: dry and wet, and distinguishing between them is important because the prognosis and required treatments vary.
The Underlying Mechanisms of Damage
The core difference between the two forms lies in the process causing macular damage. Dry AMD, accounting for 80% to 90% of all cases, is a slow, degenerative process. It is defined by the accumulation of yellowish lipid and protein deposits called drusen beneath the macula.
These waste products interfere with the retinal pigment epithelium (RPE) cells, which support photoreceptors. Over time, this leads to the thinning and death of RPE and photoreceptor cells, known as geographic atrophy (GA). GA is the advanced stage of dry AMD, causing irreversible, structural damage in a slowly expanding pattern.
Wet AMD, though less common, is more severe and involves the abnormal growth of new blood vessels. This process, called choroidal neovascularization (CNV), is stimulated by vascular endothelial growth factor (VEGF), a protein that promotes blood vessel formation.
These new vessels grow from the choroid layer beneath the retina and are fragile, causing them to leak fluid, blood, and lipids into the macula. This leakage rapidly disrupts the retinal structure, causing swelling. The fluid accumulation and subsequent bleeding lead to scar tissue formation and rapid, severe damage to central vision.
Differences in Symptoms and Progression
Dry AMD symptoms are subtle at first and progress slowly over many years. Patients notice a gradual blurring or haziness in their central vision, or they may require brighter light for reading and close work. This slow deterioration allows the condition to advance without immediate alarm.
In contrast, wet AMD is characterized by a sudden and dramatic onset of symptoms, making it an urgent medical matter. The leakage of fluid and blood causes specific visual distortions. A hallmark symptom is metamorphopsia, where straight lines appear wavy or distorted. A rapid, noticeable blind spot, or scotoma, in the central field of vision is also common. Dry AMD can transition to the wet form at any stage, requiring immediate attention, but the reverse progression does not occur.
Distinct Treatment Approaches
For dry AMD, there is currently no treatment that can reverse the damage, so the focus is on slowing progression and monitoring. Lifestyle adjustments and nutritional supplementation are the mainstays of managing intermediate and advanced dry AMD.
Specific high-dose formulations of vitamins and minerals, known as AREDS or AREDS2 supplements, are recommended for many patients. This formulation contains antioxidants like Vitamin C, Vitamin E, zinc, copper, lutein, and zeaxanthin, and has been shown to reduce the risk of progression to advanced AMD. Regular monitoring watches for any signs of conversion to the wet form.
The management of wet AMD is urgent and centers on directly counteracting the underlying cause: the abnormal blood vessels. Treatment involves anti-VEGF (anti-vascular endothelial growth factor) therapy, administered as an injection directly into the eye.
These medications block the VEGF protein, stopping the growth of new vessels and reducing the fluid leakage that causes rapid vision loss. This proactive treatment often begins with a loading phase of monthly injections, followed by a maintenance schedule tailored to the patient’s response. Anti-VEGF therapy can stabilize or improve vision if the condition is caught and treated early, requiring ongoing, frequent medical intervention to suppress the active disease process.