Mechanisms of axon-glial injury of the optic nerve.
The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myclin. The phases of symptom onset, recovery, persistence, and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory mediators; demyelination and axonal injury with recovery through plasticity and remyelination; and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage. Cell death may occur in response to a state of injury from which protection would be anticipated under more favourable neurobiological conditions. Conversely, optimal growth factor environment may save cells from otherwise lethal events occurring at the cell membrane. Hence, in the context of brain inflammation, there is an inseparable interplay between immunological and neurobiological contributions to tissue injury.
Compston
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Department of Clinical Neurosciences, University of Cambridge, Clinical School, Addenbrooke's Hospital, Hills Road, Cambridge, UK. DASCompston@aol.com
D017209:Apoptosis / Q000502:physiology; D001369:Axons / Q000502:physiology*; D003711:Demyelinating Diseases / Q000503:physiopathology; D006801:Humans; D009103:Multiple Sclerosis / Q000503:physiopathology; D009410:Nerve Degeneration / Q000503:physiopathology; D009414:Nerve Growth Factors / Q000502:physiology; D009836:Oligodendroglia / Q000502:physiology*; D009900:Optic Nerve / Q000503:physiopathology; D020221:Optic Nerve Injuries / Q000209:etiology / Q000503:physiopathology*; D009902:Optic Neuritis / Q000503:physiopathology
D009414:Nerve Growth Factors