Author:

Abstract:

Purpose Glaucoma is characterized by progressive retinal ganglion cell (RGCs) apoptosis, resulting in visual fi eld loss. Current treatment of this disease is directed towards the reduction of intraocular pressure (IOP), which is the main -but not onlyrisk factor of glaucoma. Besides IOP lowering, there is no eff ective neuroprotective therapy. So, there is a need for the development of new strategies preventing or inhibiting neuronal damage in glaucoma. " erefore, we want to investigate the neuroprotective eff ects of a local ROCK-inhibitor (AMA0076; Amakem NV) in diff erent models of neurodegeneration. Methods First, the in vitro role of AMA0076 will be tested on cultured RGCs subjected to hypoxia. At diff erent time-points after administration, cell survival and apoptosis will be assessed. Secondly, the in vivo neuroprotective eff ect of AMA0076 will be investigated in diff erent mouse models for neurodegeneration. Mice will be subjected to the optic nerve crush model and a chronic laser-induced glaucoma model to induce IOP-increase and RGCs damage. Immediately after the injury, AMA0076 will be injected into the vitreous. On diff erent time-points the number of RGCs will be determined on retinal fl at mounts and diff erent immunostainings will identify apoptosis, axon degeneration and microglial activation. Conclusion " erapy focusing solely on IOP lowering is not suffi cient to halt visual deterioration in glaucoma patients. Indeed, patients can continue losing vision despite a successful IOP-control. " erefore, new therapies concentrating on neuroprotection to prevent, hinder or even reverse RGCs death might be as important as IOP-lowering strategies. " is study on the neuroprotective role of ROCK-inhibition in glaucoma will potentially shed new light on future possibilities for neuroprotection in glaucomatous nerve damage.