Originally published July 2003
All layers of the retina age, which can contribute to loss of vision from retinal maculopathy. This is a summary of these processes. For definitions and illustrations of the retinal layers, see Anatomy of the Eye on this web site. For definitions of terms, see the MD Support Glossary.
Synchisis senilis. Gel can become more liquefied.
Syneresis. Gel can collapse in on itself, pulling on the retina at attachment points. May lead to a posterior vitreous detachment (PVD), retinal tears, and detachments at locations of macular holes.
Asteroid hyalosis. Development of calcium salts in (usually) one eye. Chance of occurence is low: 1 or 2 per thousand population.
Photoreceptor and Ganglion Cells
Oxidative stress. Cellular damage caused by reactive oxygen intermediates (ROIs) such as free radicals, peroxides, and single oxygen species. Can also occur from the presence of polyunsaturated fats and continuous exposure to light.
Cell number reduction. Rod cells (periphery) normally reduce by approximately 30% with age, leading to diminished night vision. Number of cone cells (central) normally remains fairly stable. Number of rod cells is approximately 120 million. Number of cone cells is 6.3 to 6.8 million.
Reduced blood flow. Possibly caused by accumulation of waste and retinal pigment epithelium (RPE) ischaemia. Can lead to malnutrition of the photoreceptor cells.
Drusen. Accumulation of lipids and photoreceptor cell waste material. Soft drusen can lead to neovascularization. Hard drusen is not necessarily a precursor of macular degeneration.