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Impaired Dark Adaptation: The Earliest Biomarker of AMD

Research has shown that impaired dark adaptation function can be detected at least three years before drusen are clinically evident, allowing for earlier diagnosis, treatment and monitoring of AMD.

 

 

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AMD affects the part of eye known as the macula

Age-related macular degeneration is a leading cause of adult blindness worldwide. This chronic progressive disease affects the part of the eye known as the macula. In a healthy eye, the choriocapillaris supplies oxygen and nutrients to the outer retina, which then pass through Bruch’s membrane into the retinal pigment epithelium cells. These nutrients are vital to healthy function of the photoreceptors. Vitamin A is one of these nutrients. RPE cells convert vitamin A to 11-cis retinal, which moves from the RPE cell into the rod to be used for rhodopsin regeneration. Normal rhodopsin regeneration is required for normal rod-mediated dark adaptation function and thus normal night vision.

Basal linear deposits form within Bruch’s membrane

In AMD, the RPE cells become damaged leading to the secretion of cholesterol, which becomes ubiquitous across the macula. The basal linear deposits form within Bruch’s membrane while the basal laminar deposits form between Bruch’s membrane and the RPE cells. These deposits contain the same type of cholesterol found in the carotid artery of patients with atherosclerosis. This cholesterol layer, which is not visible with imaging technology, causes oxidative stress and inflammation. It also impedes the transport of vitamin A, which impairs rhodopsin regeneration. This localized vitamin A deficiency causes impaired dark adaptation and impaired night vision. These deposits grow over time. Where the deposits become sufficiently thickened, the lesion becomes clinically detectable as a druse.

The first visible druse caused by AMD is just the tip of the iceberg

The first visible druse caused by AMD is just the tip of the iceberg of these lesions. As the lesions grow with disease progression, more drusen appear and grow larger and dark adaptation becomes further impaired. Research has shown that impaired dark adaptation function can be detected at least three years before drusen are clinically evident, allowing for earlier diagnosis, treatment, and monitoring of AMD.