Biology of AMD
What is AMD?
As a chronic, progressive disease, age-related macular degeneration (AMD) is the leading cause of adult blindness in developed countries. It occurs when fatty deposits accumulate in the retina and block absorption of nutrients, such as vitamin A, necessary for normal cell function.
AMD affects the part of the retina responsible for central vision, called the macula. As the macula deteriorates, it becomes increasingly difficult to read, recognize faces and see in dim light.
What Happens in the Back of the Eye?
Cholesterol deposits accumulate in the macula years before drusen are visible, making drusen the tip of the iceberg in AMD pathology.
Before drusen are visible, an invisible layer of cholesterol builds up between the pigmented layer of the retina (RPE) and the elastic layer of Bruch’s membrane. These cholesterol deposits—basal laminar (BLamD) and basal linear (BLinD)—cause oxidative stress and inflammation, hindering nutrient transportation to photoreceptor cells.ii As photoreceptor cells die, it becomes harder for the eyes to adjust to darkness and night vision declines. This dark adaptation impairment is the first sign of AMD.ii
Diagnosing the earliest stages of AMD can present a challenge because these patients often have good corrected visual acuity and the retina appears normal upon clinical examination. Consequently, a routine vision test may not raise any suspicion of the disease.
Subtle yet progressive, night vision difficulty is the earliest symptom of AMD. Often presented as problems seeing at night or reading in dim light, impaired dark adaptation function is the first biomarker of AMD—with impairment taking place at a subclinical level at least three years before drusen are visible.ii
No pigmentary abnormalities are apparent upon examination at this stage, and if drusen is detected, these are <63 μm.
Most people do not experience vision loss in the early stage of AMD, but night vision problems are often reported. Though no pigmentary abnormalities are apparent upon examination, medium-sized drusen (>63 μm and ≤125 μm) are present.
At this stage, some people may see a blurred spot in the center of their vision. In addition to night vision issues, these patients may also have issues with contrast sensitivity. Some pigmentary abnormalities may be observed and at least one druse >125 μm is present.
At this stage, vision loss becomes noticeable due to geographic atrophy (GA) or choroidal neovascularization (CNV).
From subclinical to advanced AMD, all stages of the disease are the manifestation of the same underlying pathology.
Using AdaptDx® to measure dark adaptation function—in conjunction with clinical examination and imaging—improves the clinician’s ability to diagnose AMD at its earliest stages. With earlier detection and treatment of AMD, we can work towards eliminating blindness caused by this chronic, progressive disease.
The AdaptDx is especially useful for optometrists and general ophthalmologists who see many patients with “normal” clinical exams, since it can detect subclinical AMD up to three years before clinical onset. With the AdaptDx, you will be in the front line in detecting these patients and will be able to carefully monitor and treat those with subclinical AMD.