RAGE and its ligand amyloid beta promote retinal ganglion cell loss following ischemia-reperfusion injury.

Introduction: Glaucoma is a progressive neurodegenerative disease associated with age. Accumulation of amyloid-beta (Aß) proteins in the ganglion cell layer (GCL) and subsequent retinal ganglion cell (RGC) loss is an established pathological hallmark of the disease. The mechanism through which Aß provokes RGC loss remains unclear. The receptor for the advanced glycation end product (RAGE), and its ligand Aß, have been shown to mediate neuronal loss via internalizing Aß within the neurons. In this study, we investigated whether the RAGE--Aß axis plays a role in RGC loss in experimental glaucoma. Methods: Retinal ischemia was induced by an acute elevation of intraocular pressure in RAGE [ABSTRACT FROM AUTHOR]