Loss of vision in the ageing eye

Age and Ageing, March, 1997 by A.J. Bron

The effects of ageing on the retina

Professor John Marshall (Frost Professor of Ophthalmology, UMDS, London) indicated that by the year 2050, about 3 million of the UK population and 15 million in the US will be over the age of 85 years. This very old population has a 30% risk of losing vision as a result of ARMD.

Genetic factors may be involved in all forms of ageing, but in non-dividing cells (such as those of the RPE) the effects of cumulative stresses are extremely important. For the retina, optical radiation in the wavelengths between 400 and 1400 nm provides a stress which generates oxidative changes in the tissue. The cones are more susceptible to chronic low levels of radiation, whereas the RPE is more vulnerable to short bursts of high intensity. For both, the blue end of the spectrum is the most damaging. In the visual process, light is absorbed by visual pigments in the outer segments of the rod and cone photoreceptors. The turnover of the discs which make up the rod outer segments is rapid, and is modulated by light. Rod discs are phagocytosed by the adjacent RPE in the early hours of the morning, and the complete stack of discs is turned over once every 2 weeks.

With ageing, the lipid products of phagocytosis accumulate within the RPE as the age pigment lipofuscin. It has been postulated that in old age, this material is released from the RPE and renders the overlying Bruch's membrane hydrophobic. Thus the transport of water and other materials across the membrane and between the retina and the choroidal circulation is impaired. It is also envisaged that light-induced stress to the RPE cells may impair their ability to digest outer segment discs and therefore hastens the process of damage to Bruch's membrane.

With age, deposits (drusen) appear in Bruch's membrane in the region of the macula, and represent a risk factor for ARMD. It is thought that they stimulate invasion by macrophages, followed by new vessels which pass across Bruch's membrane into the subepithelial space. Fluid leakage, exudate and haemorrhage can then cause catastrophic loss of central vision.

More work is needed to determine the genetic and environmental factors responsible for ARMD. Ways are needed to stimulate the phagocytic capacity of the RPE or prevent build-up of hydrophobic materials within Bruch's membrane. Current clinical approaches include the prophylactic use of lasers, but pharmacological approaches are also being considered.

ARMD

Mr T. ffytche (Consultant Ophthalmologist, St Thomas's and Moorfields Eye Hospitals, London) detailed the clinical manifestations of ARMD. The early symptoms of macular disease include metamorphopsia (distortion of vision), micropsia, macropsia, and delayed recovery after exposure to bright lights (so that the headlights of oncoming cars may make night driving very difficult). Eventually a central scotoma makes reading and fine manipulations requiring vision almost impossible, though navigational ability remains. Patients with loss of central vision in one eye have a 50% chance of developing similar problems in the other eye within 5 years.