Abstract

Age-related decrements in acuity and contrast sensitivity are only partially explained by the combined effects of pupillary constriction and lens opacification. The notion of a neural origin for these visual deficits remains controversial. Limited quantitative data on photoreceptors in aging suggest disorganization of both rod and cone outer segments, displacement of nuclei, and outright cell loss, particularly in the fovea. The relationship of these phenomena to nonpathological changes in retinal supporting tissues which may impair transport of nutrients across the outer blood–retinal barrier is unclear. The effects of age-related point deletions in the photoreceptor mosaic on spatial sampling characteristics of the retina are unknown. Recent studies of photoreceptor distribution in human retina show that individual variability in foveal cone density is much greater than previously appreciated. The implications of this finding for aging studies are (1) sample size must take into account high variability; (2) anatomical data need to be viewed in relation to functional and clinical data from the same individual; (3) photoreceptor counts alone are probably not sufficiently sensitive to detect age-related cell loss, and some measure of mosaic disorder is likely to be more informative.

© 1986 Optical Society of America