Purpose: To assess the similarities and differences in retinal microvascular function between mild Alzheimer’s disease (AD) patients, early-stage primary open angle glaucoma (POAG) patients and healthy controls. Methods: Retinal vessel reactivity to flickering light was assessed in 10 AD, 19 POAG and 20 healthy age matched control patients by means of dynamic retinal vessel analysis (DVA, IMEDOS, GmbH, Jena, Germany) according to an established protocol. All patients additionally underwent BP measurements and blood analysis for glucose and lipid metabolism markers. Results: AD and POAG patients demonstrated comparable alterations in retinal artery reactivity, in the form of an increased arterial reaction time (RT) to flicker light on the final flicker cycle (p = 0.009), which was not replicated by healthy controls (p > 0.05). Furthermore, the sequential changes in RT on progressing from flicker one to flicker three were found to differ between healthy controls and the two disease groups (p = 0.001). Conclusion: AD and POAG patients demonstrate comparable signs of vascular dysfunction in their retinal arteries at the early stages of their disease process. This provides support for the concept of a common underlying vascular aetiology in these two neurodegenerative diseases.

Glaucoma is a group of progressive optic neuropathies characterized by retinal ganglion cell (RGC) loss, optic nerve head damage and corresponding visual-field loss. Intraocular pressure (IOP) is the principal modifiable risk factor, and lowering IOP remains the only treatment approach that has been shown in randomized clinical trials to slow glaucomatous progression, including in normal-tension glaucoma (NTG). However, IOP reduction does not eliminate progression in all patients, indicating that susceptibility to pressure-related damage is heterogeneous and that additional biological mechanisms are relevant. This review examines current and emerging pharmacological strategies for IOP lowering, approaches intended to protect RGCs independently of IOP, and the methodological problem of demonstrating neuroprotection in clinical trials.