Retinal ganglion cell loss in postmortem tissue of Alzheimer disease, glaucoma, and healthy normal subjects Loss of retinal ganglion cells (RGCs), the hallmark of glaucoma (GL), is also thought to occur in patients with Alzheimer disease (AD). 1,2 Structural measures derived with optical coherence tomography have been used as proxies for RGC estimates in GL 3,4 and AD, 5 both independently and in comparative studies. 6,7 Although optic nerve damage in GL 8,9 and AD 10 has been reported in postmortem tissue, quantification in the retina is limited to the use of generic techniques, such as Nissl staining in the ganglion cell layer, 11,12 which label all nuclei and not specifically RGCs. Depending on retinal eccentricity, the percentage of displaced amacrine cells, which are also present in the ganglion cell layer, can range from 3% to 80%. 13 The objectives of this study were to confirm specific RGC loss in AD, and how this compared with GL and healthy aging in normal (NL) eyes. Ethics approval was acquired from the Nova Scotia Health Authority Research Ethics Board. Postmortem paraffin-embedded retinal sections were obtained from the Human Eye Biobank for Research (Toronto, Ont.). Disease status was provided for 9 de-identified subjects. The mean (standard deviation [SD]) age of the AD, GL, and NL subjects was 73 (2), 74 (4), and 74 (2) years, respectively. In each group there were 2 females and 1 male. Anteroposterior retinal sections were deparaffinized, underwent heat-induced epitope retrieval, and were prepared for immunohistochemistry. RGCs were labelled with the RNA binding protein with multiple splicing 14 antibody, amacrine cells were labelled with the cholinergic acetyltransferase antibody, and nuclei were labelled with 4 0 ,6-diamidino-2-phenylindole. Fluorescence micrographs were acquired with an epifluorescence microscope (Zeiss Axio
