Ischemia of the inner retina, caused by the presence of naked or acellular vessels (formed from a thickening of the basal membrane of the capillaries), will be aggravated by the difficulty of diffusion of nutrients across the inner limiting membrane, and the elimination of catabolites. In the group of people with AMD, the changes are more severe than those in normal individuals of the same age. The changes to the inner retina in individuals with AMD are equivalent to those of the outer retina and represent an advanced aging of the retina. In the studied group of patients with AMD, the basal membrane of the retinal capillaries is considerably thicker than that of normal individuals of the same age with a thick external layer of collagen in contact with the astrocytes and Miiller cells. The number of acellular capillaries is higher, especially in cases of AMD in patients aged over 81. In fact, the ischemia that establishes itself in these cases is considerably worse than that of healthy individuals of the same age. In all cases of AMD, there is an elevated number of hypertrophic and reactive astrocytes. Under an electron microscope, it has been seen that these astrocytes phagocyte the residues of the necrotic or apoptotic dead ganglion cells. The astrocytes contain elevated quantities of lysosomes and lipofuscin, as do the ganglion cells and their axons.
The extended retinal ischemia seen in patients with AMD, together with the loss of astroglial cells that occurs with normal aging, cause the death of ganglion cells that are not protected against oxidative stress. Furthermore, the basal membrane of the inner limiting membrane in AMD becomes thicker than that of healthy individuals of the same age, obstructing the metabolic exchange between the retina and the vitreous humor. The reactive astrocytes are overfilled with electron dense material and expel this material into the inner limiting membrane. In all the individuals with AMD, strongly GFAP+ trunk-shaped astroglial protrusions have been found that cross the inner limiting membrane and enter the vitreous humor. These protrusions are formed of astrocytes with long protrusions parallel to the inner limiting membrane and form a glial membrane. Under an electron microscope, cells have been observed in the vitreous humor, and judging by their ultrastructural properties, they could be astrocytes. These cells possess a clear cytoplasm, a large number of cellular organelles, and dense glial filaments. The protrusions of these cells intercommunicate across many gap junctions. The astrocytes also possess microvilli in contact with the vitreous humor, where there is no basal membrane, allowing direct contact between the vitreous humor and the astrocytes. These cells have ultrastructural characteristics similar to the epiretinal membranes observed in other pathologies. Another type of cell that also has been observed more often, is highly GFAP+ and column-shaped, and lies parallel to the inner limiting membrane, which can be confused with the aforementioned astro-cytes. The morphological characteristics of these cells is reminiscent of the Miiller cells as they are more robust, column-shaped, and have few protrusions. These cells should be reactive Miiller glia, which in pathologic situations express the GFAP.
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