Glaucoma and the brain: Trans-synaptic degeneration, structural change, and implications for neuroprotection.

Mitchell Lawlor, Helen Danesh-Meyer, Leonard A Levin, Indran Davagnanam, Enrico De Vita, Gordon T Plant

Journal: Survey of ophthalmology 2018;63(3):296-306

PMID: 28986311

Full Text on Elsevier Science View on PubMed

Abstract

A recent hypothesis to enter the literature suggests that glaucoma is a neurodegenerative disease. The basis for this has been the finding of central nervous system changes in glaucoma patients on histology and neuroimaging. It is known that retinal ganglion cell pathology of any cause leads to anterograde and retrograde retinal ganglion cell degeneration, as well as trans-synaptic (transneuronal) anterograde degeneration. Trans-synaptic degeneration has been demonstrated in a range of optic neuropathies including optic nerve transection, optic neuritis, and hereditary optic neuropathies. More recently, similar changes have been confirmed in glaucoma patients using the neuroimaging techniques of voxel-based morphometry and diffusion tensor imaging. Some studies have reported brain changes in glaucoma outside the retino-geniculo-cortical pathway; however, these are preliminary and exploratory in nature. Further research is required to identify whether the degenerative brain changes in glaucoma are entirely secondary to the optic neuropathy or whether there is additional primary central nervous system pathology. This has critical implications for neuroprotective and regenerative treatment strategies and our basic understanding of glaucoma.

Address: Save Sight Institute, Discipline of Clinical Ophthalmology and Eye Health, University of Sydney, Sydney, New South Wales, Australia; Department of Neuro-Ophthalmology, Moorfields Eye Hospital, London, United Kingdom. Electronic address: [email protected].; Department of Ophthalmology, University of Auckland, Auckland, New Zealand; University of Melbourne, Parkville, Victoria, Australia.; Departments of Ophthalmology and Neurology & Neurosurgery, McGill University, Montreal, Quebec, Canada; Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, Wisconsin, USA.; Department of Neuro-Ophthalmology, Moorfields Eye Hospital, London, United Kingdom; Academic Neuroradiological Unit, Department of Brain Repair & Rehabilitation, UCL Institute of Neurology, London, United Kingdom; Lysholm Department of Neuroradiology, National Hospital for Neurology and Neurosurgery, UCL Hospitals Foundation Trust, London, United Kingdom.; Academic Neuroradiological Unit, Department of Brain Repair & Rehabilitation, UCL Institute of Neurology, London, United Kingdom; Lysholm Department of Neuroradiology, National Hospital for Neurology and Neurosurgery, UCL Hospitals Foundation Trust, London, United Kingdom; Department of Biomedical Engineering, King's College London, London, United Kingdom.; Department of Neuro-Ophthalmology, Moorfields Eye Hospital, London, United Kingdom; Department of Neuro-Ophthalmology, National Hospital for Neurology and Neurosurgery, London, United Kingdom; The Medical Eye Unit, St Thomas' Hospital, London, United Kingdom.

DOI: 10.1016/j.survophthal.2017.09.010

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MeSH Terms: Brain, Glaucoma, Humans, Neurodegenerative Diseases, Neuroprotection, Neuroprotective Agents, Retinal Ganglion Cells, Synapses, Visual Pathways