Choroidal neovascularization in age-related macular degeneration - What is the cause?

A central measure of the qualtiy of a hypothesis is its ability to explain known observations. Although some elements of senescence and ischemia theories may be operative, the oxidative injury model as we propose above seems to explain injury model as we propose above seems to explain the observed aspects of CNV, and geographic atrophy, in ARMD. Each of the aspects of the proposed theory is biologically plausible and has been based on experimental data, some of which are related to the eye and some to other fields such as atherosclerosis and cancer research. There are still a number of questions that face all of those diseases in terms of prevention and treatment. Although aging, in part may be the result of an accumulation of genetic defects that do not necessarily inhibit reproduction, there is increasing evidence that much of the aging phenotype is also the result of oxidatives stress and the induced cellular adaptation responses. A principle risk factor for degenerative aspects of aging appears to be life itself. Aging is a problem that has challenged biologists and philosophers for centuries. Aging has deterministic and stochastic aspects, something that most ancient of philosophers knew. Clearly, there are numerous factors involved, and many of these are coded into our genetic structure. Certainly, genes are powerful navigators of our face, but the course can be modified by our interventions. ARMD affects the quality of life, particularly in aged people who may have other infirmities. We are closing in on a workable hypothesis for CNV in ARMD; it is easily conceivable that there will be a viable theory in the next few years. The next step is to identify points of attack on the process so that ARMD may be prevented or cured.