This open access paper examines what is known of the aging of the retina, and notes the difficulties inherent in relating any of those changes to specific declines in vision. The research community has an increasingly detailed view of exactly what differentiates an old retina from a young retina, structurally, chemically, and in the changing behavior of the various types of cell that make up retinal tissue. It is a challenge to relate data obtained in laboratory animals to loss of specific aspects of visual function, however, particularly the more subtle ones. One can’t ask mice and rats to sit through the same test procedures as humans undergo, and obtain useful feedback via that approach.
Visual aging is linked to a decline in functional activity causing lower visual acuity, lower contrast sensitivity and impaired dark adaptation. However, although it has been reported that the age-related visual impairment is mainly due to a neuronal malfunction together with cell loss, the specific reasons of aging are still uncertain. How, and at what level, are the diverse neuronal populations affected? And how much are other retinal players involved?
By characterizing retinal aging in experimental animals (pigmented and albino rats) under controlled and healthy conditions, we found that the retinal function, as measured with full field electroretinograms, decreased ~50% at 22-months compared with 2-month-old rats. Whether neuronal malfunction or cell loss is mainly responsible for this reduced functionality is still an open question, even though structural changes in the optical components may contribute to this reduction. Interestingly, several studies suggest cell loss based on the retinal thinning that occurs with aging. However, although when we measured the retinal layers in vivo we observed a decrease in thickness ~14%, we also saw that the constant retinal growth was responsible for the retinal thinning, since volumetric and quantification analyses indicated that the thinning did not involve neuronal loss.
The retina is a highly organized and specialized tissue. The light-sensitive photoreceptors are essential for an effective signal transduction and to initiate the efficient transmission of impulses through the retina. They are vulnerable to light-induced damage and many publications have shown the degeneration of outer segments during aging. The central retina probably receives greater light exposure triggering different metabolic requirements that increases metabolic stress. In fact, a deficiency in DNA repair enzymes, damage induced by excitatory amino acids, specific age-related metabolic changes, a general decline in autophagy activity, and reduced energy production by mitochondrial metabolism collectively result in oxidative stress that may affect photoreceptor functionality. All that in addition to lipofuscin accumulation, morphological alterations and damage in the retinal pigmented epithelium accompanied by a para-inflammatory response are the signature signs of aging in the retina.
To preserve visual function, the eyes and brain require precisely tuned machinery. Any of the above-mentioned changes related to aging, including synapse remodelling or neuronal loss in response to age may contribute or play a crucial role in the continuous and irreversible decline in vision. Importantly, age may end causing a partial or complete distorted image formation, more so in a timeframe where our lifespan is increasing. So, could this retinal dysfunction be prevented or restored?