Most studies of age-related macular degeneration (AMD) have focused on the outer retina but little has been done on the involvement of astrocytes in this disease. We examined normal (young and old) and pathological (AMD) human retinas for the presence of changes in morphology and distribution of the astrocytes. Electron microscopy and inmunohistochemical techniques (anti-GFAP) were used for this study. Astrocytes in the ageing group showed: (1) higher GFAP immunoreactivity and more cytoplasmic organelles and glial filaments than astrocytes from younger retinas; (2) lipofucsin deposits; (3) a significantly smaller number of cells in the honeycomb astroglial plexus in the ganglion cell layer than in the younger group; and (4) Spaces with no GFAP reactivity in the nerve fiber layer. Changes observed in the AMD group were: (1) the basal membrane of the retinal capillaries was considerably thicker than in normal old individuals; (2) There were numerous non-functional capillaries; (3) There were hypertrophic astrocytes that phagocytosed dead ganglion cells; and (4) There were glial membranes constituted by astrocytes and Müller cells located between the vitreous humour and internal limiting membrane. These observations suggested that the extensive retinal ischaemia that can occur with AMD, together with the loss of astroglial cells accompanying normal ageing, could cause the death of the ganglion cells which cannot be protected from oxidative damage. Extensive ischaemia could cause the astrocytes to migrate to the vitreous humour where there is a metabolic reserve.
(C) 2001 Academic Press.