title: Glaucoma, apoptosis, and neuroprotection.
abstract: The demise of the retinal ganglion cell represents the final common pathway of glaucomatous vision loss. Various studies demonstrate that ganglion cells die by the mechanism of apoptosis in conditions such as experimental animal models of glaucoma and optic nerve transection, and in human glaucoma. Apoptosis is a basic cell death mechanism noted in a number of neurodegenerative conditions. It constitutes a genetically coded "suicide" program activated when cells are no longer needed or have been seriously damaged, and is typified by rapid phagocytosis without inflammation. These cells demonstrate characteristic morphological changes on electron microscopy: nuclear chromatin condensation, compaction of cytoplasmic organelles, and membrane blebbing. Neurotrophin withdrawal and excitotoxic neurotransmitters have been implicated in apoptosis in ganglion cells damaged by glaucoma. Understanding the cellular and molecular biological events involved in ganglion cell death may lead to novel approaches to the treatment of glaucoma.
authors.affiliation: Department of Ophthalmology, Johns Hopkins Hospital, Baltimore, MD 21287-9289, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: McKinnon
mesh_terms: D000818:Animals; D017209:Apoptosis; D001766:Blindness / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D002470:Cell Survival; D015316:Genetic Therapy / Q000379:methods*; D005901:Glaucoma / Q000150:complications / Q000473:pathology / Q000517:prevention & control; D006801:Humans; D009900:Optic Nerve / Q000473:pathology*; D012165:Retinal Ganglion Cells / Q000473:pathology*