AMD is the most common cause of blindness in the developed world. The macula is the central portion of the retina responsible for colour vision, reading and fine detail clarification. As the name suggested, the incidence of AMD increases with age and the macular region is primarily affected.

Classification of AMD

There are two main types, the atrophic or dry type and the exudative or wet type. The dry type is more common and fortunately, it is the benign form of the condition. The progression tends to be slow and it affects reading vision preferentially.

The wet type is less common but visual loss is substantial. It is usually first presented with distortion and followed by substantial loss of central vision. Often described as a "thumb print on the center of vision". The distortion is caused by the formation of the abnormal new vessel complex behind the retina, this is often referred as the "membrane" as it was originally called subretinal neovascular membrane (SRNVM). The complex is now known to be originated from the choroid, which is the vascular coat of the eye, hence it is now called choroidal neovascularization (CNV). The CNV can bleed causing substantial retinal damage.

Current therapies of AMD

If the CNV locates some distance away from the fovea which is the center of the macula. The CNV can be destroyed by laser. Unfortunately, most patients came too late to be treated when the first eye is affected. As distortion is the most consistent symptom for CNV, affected patients would commonly be asked to look for distortion in their good eye on a daily basis.

If the CNV is very close to or in fact behind the fovea, laser treatment might not be most appropriate. Although the long term vision (i.e. after 2 years) might be better with laser therapy, the vision can drop substantially right after the laser. This sudden drop of vision does not allow time for the patient to adapt to the change of life style. Most surgeons would be very reluctance to laser at this stage. Subretinal surgery to remove of the CNV has been attempted but the results were poor for AMD.

Photodynamic therapy (PDT) has been used to treat a group of patients with the so called “predominantly classic CNV”. You would need to see a retinal specialist to determine whether you would be suitable for treatment or not. This treatment can slow the disease process but seldomly improve vision.

In reality, once CNV is developed, it is probably too late. The management of AMD is still mainly the use of low visual aids, from simple magnifiers to CCTV.

Pathogenesis of AMD - Genetic or Environment

There is increasing evidence to suggest that AMD is genetically determined but affected by environment. It has been noted in many studies for some years that exudative AMD is much less common in blacks. However, the most convincing evidence came from twins and siblings studies where the fundus appearances between twin and sibling pairs are so strikingly similar. There are very few people would deny the importance of genetics. Furthermore, there is an increasing incidence of AMD in Japan. However, the pattern of AMD is significantly difference with a high incidence of pigment epithelial detachment (PED). It is likely that there are more than one gene involved in AMD. There might be one or more genes determine the atrophic type of AMD, another gene or genes determine exudative AMD and another gene or genes determine the PED. If this hypothesis is true, then the Japanese might have a high incidence of the PED gene(s) whilst the whites have the exudative AMD gene(s).

On the other hand, the increasing incidence of the AMD in Japan also signifies the importance of environmental factors. Over the past 20 years, the Japanese society has been "westernised". It is possible that the abnormal gene requires a trigger to initiate the disease. Some environmental factors associated with the westernised way of life might be the necessary trigger. That can also explain the twin and sibling studies might not be exclusive genetically determined, as there are no significant difference of the environment between the studied pairs.

Future potential therapies in AMD

As I mentioned before, once CNV is formed, prognosis is poor and treatment is usually ineffective. In the future, the most significant therapy will be in the prevention of CNV and hence visual loss. It would be very useful if the CNV gene(s) are identified and hence we can treat the high risk patients early. There are a few different approaches. There is evidence to suggest that the function of the retinal pigment epithelial (RPE) cells deteriorate with age and there are also thickening of and breaks in the Bruch membrane with AMD. It is well known that CNV is commonly associated with breaks in the Bruch membrane. Transplantation or "freshening" of the RPE cells have been suggested but it has to be carried out at an early stage of the disease. The current attempt of RPE transplantation in end-staged AMD might be useful to prove the feasibility of the technique, but it is of no benefit to patients. Another approach is to alter the composition of the Bruch membrane and prevents breaks in the membrane. This latter work is proved to be difficult and funding is relatively restricted.