The notion of AMD, or age-related macular degeneration, is commonplace. It is a consequence of aging and represents a vexing degenerative process because it is so challenging to treat. The crystalline lens of the eye doesn’t garner as much attention in aging because cataract surgery and implantation with IOLs has become so commonplace, and in most cases so successful. Cataract is best conceived as lenticular degeneration, what I’ve previously proposed to call ALD and the anterior counterpart of AMD.
The Gulden Ophthalmics cataract (ALD) model is an effective chairside communication aid that models what happens to the crystalline lens in various types of cataract. We reassure patients that cataract is not a growth, but a clouding of the natural lens inside the eye. And when that cloudy lens interferes with visual function, the surgeon will extract the old lens and implant a new one. Out with the old and in with the new.
But what causes the lens to degenerate and become cloudy in the first place? The easiest explanation for patients to understand is that the lens in the eye contains proteins, and when those proteins denature it’s like a film that forms within a glass of milk left overnight without being rinsed properly – the film is the protein in the milk that has denatured.
As the filmy crystalline lens progresses to the yellowy-brown brunescent phase, it’s like newspaper that has been left in the sun too long. In that instance, it is the cellulose and lignin that are denaturing as a result of an oxidative process triggered by excessive sunlight exposure.
In fact, some authorities on aging and degenerative processes have noted that the primary type of protein deposition in the lens in patients with Alzehimers disease is beta amyloid protein – the same process that occurs in the brain. This is not entirely surprising when we remind ourselves that the eye is part of the brain. In a neat article in Review of Optometry, Dr. Paul Ajamian quotes Dr. Clement Trempe – an ophthalmologist on staff at The New England Eye Institute and faculty member at NECO, that a unique cataract presentation with characteristic fibrils seen under high magnification can be one of the earliest identifiable biomarkers of Alzheimers.
So when is the “right” time to treat ALD? As previously noted, it’s when the degenerative process interferes with visual function. But how do we gauge that?