One possible mechanism is the selective vulnerability of rods. One explanation for the higher vulnerability of rods with respect to cones is the fact that the acromere disks of the rods have a higher rate of renewal. This requires a notable energy expense by the rods for the renewal of the disks and by the RPE for the disposal of the old ones (Owsley et al., 2000). The RPE are responsible for the integrity of the photoreceptors, and it has been seen that the age-related changes of the photoreceptors independent of those of the RPE are slight. For example, an RPE dysfunction causes a slowdown of the rate of renewal of the photopigments in both the cones and the rods, and an increase in the convolution of the acromeres of the rods.
The principal age-related changes to the RPE are the accumulation of lipofuscin and the reduction of the granules of melanin, which is concomitant with the thickening and the accumulation of deposits in the Bruch's membranes. It has been observed that the accumulation of intracellular lipofuscin significantly reduces the function of the photoreceptors. High levels of lipofuscin have been correlated with a low number of photoreceptors in the retina. As lipofuscin is tightly related with the rods, the loss of rods should be highest in the ring with the highest density of rods, 3 to 5 mm from the center of the fovea. On the contrary, the results of Curcio et al. (1993) placed the rod loss closer to the fovea, at 0.5 to 3 mm, contradicting the correlation between the accumulation of lipofuscin and the loss of photoreceptors.
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