Purchase this article with an account.
P. Gouras, L. Ivert, M. Neuringer; Insights Into the Pathogenesis of Age-Related Drusenoid Maculopathy in Monkeys With Comparisons to Age-Related Macular Degeneration in Man. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3434.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To understand the pathogenesis of age related drusenoid maculopathy in Macaca mulatta at the electron microscopic level and compare it to what is known about age related macular degeneration in man.
Specimens from seven monkeys (19-28 years of age), six with drusenoid maculopathies and one without, as confirmed ophthalmoscopically, were obtained from two different colonies of rhesus monkeys. Tissues were rapidly fixed, then later prepared for and examined by electron microscopy.
Affected eyes showed multiple drusen, mainly in the macula, extending from 3 to 300 microns. The drusen were external to the basal lamina of the epithelium and contained cellular and/or granular debris. The cellular material arose from budding and suspected disconnection of segments of basal epithelial cytoplasm from the host cell together with a thickened basal lamina. Macrophages were seen in the inner collagen layer of Bruch’s membrane near drusen, when cellular material was present. The epithelial cells at the apex of drusen were smaller, had less lipofuscin, probably due to loss of cytoplasm, were sometimes atrophic and occasionally were migrating from the layer. A few cells showed lipoidal degeneration. There was no photoreceptor loss.
Monkey drusen seem formed by the degeneration of basal cytoplasm of the epithelium with a thickened basal lamina budding into Bruch’s membrane (see also Ishibashi et al, IOVS 27:184, 1986). These cytoplasmic buds degenerate to form granular drusen, perhaps by macrophage action. This budding hypothesis corresponds to Burns & Feeney’s report on the pathogenesis of human drusen by electron microscopy (Tr Am Ophth Soc 78:206, 1980). The latter did not find basal lamina around these buds, perhaps due to a less ideal status of human versus monkey material. Macrophage invasion was not noted by Ishibashi et al or Burns & Feeney but has since been observed in human material (Killingsworth et al, Eye 4:613, 1990; Hageman et al Prog Retn Eye Res 20:705, 2001). Therefore from an electron microscopic perspective these two diseases share a similar pathogenesis
This PDF is available to Subscribers Only