PART II: AMD - Age Related Blindness and Light
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 this oxidative debris which is itself phototoxic. 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.
Exposure to bright light can overpower the protective anti-oxidative
mechanisms in the retina. Excessive light exposure induces the
formation of lipofuscin, the oxidative debris that develops within
retinal cells, and drusen, the oxidative debris that forms in the
extra-cellular space between the monolayer of cells in the retinal pigment
epithelium (RPE) and Bruch’s membrane. Bruch’s membrane is a membrane
barrier adjacent to the RPE that separates the retina from the blood
vessels that service the retina.
Drusen is a photo-oxidative by-product that 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 destroying photoreceptor and RPE cells, and attacking the
integrity of the Bruch’s membrane. This "blue light hazard" is compounded in
the aged eye because in humans the anti-oxidative protective mechanisms
start to deteriorate at about 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, have high concentrations
of polyunsaturated fatty acids which are extremely susceptible to
peroxidation, and contain a number of potential photosensitizers.
While "Bright Light" therapy has only been widely used for about ten years and its
connection to AMD remains unproven, 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. Recently, the molecular pathways by which
light-induced oxidative damage produces the drusen which leads to AMD has been described. This establishes the
connection between the repetitious insults to the retina from damaging
levels of visible light exposure and the development of AMD. FOR THERAPISTS AND EYE SAFETY EXPERTS: A MORE TECHNICAL AND COMPLETE DISCUSSION OF THE ROLE OF LIGHT IN THE PATHOGENESIS OF AMD please click Blue Light and AMD) |