Optic nerve degeneration in experimental autoimmune encephalomyelitis

John Guy

Research output: Contribution to journalShort surveypeer-review

21 Scopus citations


The mechanisms of axonal and neuronal degeneration causing disability in optic neuritis and multiple sclerosis are poorly understood. Here we describe the role of mitochondria, oxidative stress and the effects of modulating antioxidant gene expression in the optic nerves of mice induced with experimental autoimmune encephalomyelitis, with a focus on long-term neuroprotection. Oxidative injury to the mitochondrion began prior to inflammatory cell infiltration and continued. It affected subunits of the respiratory chain, glycolysis and a chaperone critical to the stabilization and import of proteins. Oxidative products were associated with loss of membrane potential, mitochondrial degeneration and severe axonal loss. Reductions in ATP synthesis were even greater than those associated with mitochondrial diseases. Increasing SOD2 levels by viral mediated gene transfer rescued ATP synthesis, suppressed myelin fiber injury and increased retinal ganglion cell survival 1 year later.

Original languageEnglish (US)
Pages (from-to)212-216
Number of pages5
JournalOphthalmic Research
Issue number3-4
StatePublished - Apr 1 2008
Externally publishedYes


  • Experimental autoimmune encephalomyelitis
  • Gene therapy
  • Mitochondria
  • Multiple sclerosis
  • Optic neuritis
  • Oxidative stress

ASJC Scopus subject areas

  • Ophthalmology


Dive into the research topics of 'Optic nerve degeneration in experimental autoimmune encephalomyelitis'. Together they form a unique fingerprint.

Cite this