title: The molecular basis of retinal ganglion cell death in glaucoma.
abstract: Glaucoma is a group of diseases characterized by progressive optic nerve degeneration that results in visual field loss and irreversible blindness. A crucial element in the pathophysiology of all forms of glaucoma is the death of retinal ganglion cells (RGCs), a population of CNS neurons with their soma in the inner retina and axons in the optic nerve. Strategies that delay or halt RGC loss have been recognized as potentially beneficial to preserve vision in glaucoma; however, the success of these approaches depends on an in-depth understanding of the mechanisms that lead to RGC dysfunction and death. In recent years, there has been an exponential increase in valuable information regarding the molecular basis of RGC death stemming from animal models of acute and chronic optic nerve injury as well as experimental glaucoma. The emerging landscape is complex and points at a variety of molecular signals - acting alone or in cooperation - to promote RGC death. These include: axonal transport failure, neurotrophic factor deprivation, toxic pro-neurotrophins, activation of intrinsic and extrinsic apoptotic signals, mitochondrial dysfunction, excitotoxic damage, oxidative stress, misbehaving reactive glia and loss of synaptic connectivity. Collectively, this body of work has considerably updated and expanded our view of how RGCs might die in glaucoma and has revealed novel, potential targets for neuroprotection.
authors.affiliation: Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec, Canada.
authors.forename: Mohammadali
authors.initials: M
authors.lastname: Almasieh
authors.forename: Ariel M
authors.initials: AM
authors.lastname: Wilson
authors.forename: Barbara
authors.initials: B
authors.lastname: Morquette
authors.forename: Jorge Luis
authors.initials: JL
authors.lastname: Cueva Vargas
authors.forename: Adriana
authors.initials: A
authors.lastname: Di Polo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D001370:Axonal Transport / Q000187:drug effects; D018450:Disease Progression; D004285:Dogs; D005901:Glaucoma / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D051379:Mice; D009414:Nerve Growth Factors / Q000494:pharmacology / Q000627:therapeutic use; D011817:Rabbits; D051381:Rats; D020917:Receptor, trkA / Q000378:metabolism; D012160:Retina / Q000187:drug effects; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*
chemical_list: D009414:Nerve Growth Factors; D020917:Receptor, trkA