Age-Related Macular Degeneration (AMD) is the leading cause of blindness in North America.
Repeated exposure to high levels of light combined with the deterioration of anti-oxidative protective mechanisms that occurs
with age contribute to the development of oxidative debris within the retina and in the region immediately adjacent to it.
AMD results from the accumulation of some of this oxidative debris being deposited along the blood-retinal barrier which inhibits
the flow of oxygen and nutrients to photoreceptor cells, and limits the transfer of waste material from the retina into the blood stream.
Some investigators link the development of AMD with the levels of visible light exposure for at least the twenty year period before
symptoms emerge. More recently, evidence indicates that increasing daily exposure to blue visible light of young adults may advance
the onset of AMD by 10 years.
Over a lifetime, exposure to light, particularly visible blue wavelengths of light, can overpower the protective
anti-oxidative mechanisms in the retina. Excessive light exposure induces the formation of lipofuscin, oxidative debris that
develops within retinal pigment epithelium (RPE) cells, a monolayer of cells located between the photoreceptor cells and Bruch's
membrane. Bruch's membrane is a structure adjacent to the RPE that separates the retina from the blood vessels that service the
photorecptor cells and the RPE. Oxidative stress within RPE cells results in the formation of drusen, which forms in the
extra-cellular space between the retinal pigment epithelium (RPE) and Bruch's membrane. Drusen also appears to contain oxidative
debris generated in photoreceptor cells and and RPE cells.
Drusen, which contains photo-oxidative by-products, accumulates between the retinal pigment epithelium and Bruch's
membrane. Drusen formation is an early indication of AMD. Drusen and lipofuscin contain phototoxic chromophores that generate radical
oxygen species (ROS) when they absorb the blue wavelengths in visible light. These ROS induce additional damage by causing the death
of photoreceptor cells and RPE cells, and attacking the integrity of the Bruch's membrane. The "blue light hazard" is compounded in
the older eye because in humans the anti-oxidative mechanisms protecting the retina start to deteriorate significantly around age 40.
Photoreceptor cells and cells of the RPE are not replicated after birth. It is therefore inevitable that there
is a build up of oxidative debris within these cells which are exposed to high levels of light energy and high concentrations
of oxygen, and have high concentrations of polyunsaturated fatty acids which are extremely susceptible to oxidation.
Vision deteriorates with age. Most people who live over 90 years will experience Age-related Macular Degeneration. The accumulation of phototoxic debris from oxidative damage combined with the diminishing capability of anti-oxidative mechanisms that occurs with age is instrumental in the initiation of the damage to retinal tissues that leads to photoreceptor cell death and AMD.
There is a growing understanding of the molecular pathways by which light-induced oxidative damage produces the drusen which leads to AMD. The connection between the cumulative insults to the retina from exposure to damaging levels of blue visible light exposure and the development of AMD can now be established. Read more
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FOR THERAPISTS AND EYE SAFETY EXPERTS: For a more technical and complete discussion of the role of light in the pathogenesis of AMD - please see Blue Light and AMD
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