Optic nerve degeneration in experimental autoimmune encephalomyelitis

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

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
Pages (from-to)212-216
Number of pages5
JournalOphthalmic Research
Volume40
Issue number3-4
DOIs
StatePublished - Apr 1 2008
Externally publishedYes

Fingerprint

Nerve Degeneration
Autoimmune Experimental Encephalomyelitis
Optic Nerve
Mitochondria
Adenosine Triphosphate
Mitochondrial Diseases
Optic Neuritis
Viral Genes
Retinal Ganglion Cells
Mitochondrial Membrane Potential
Wounds and Injuries
Glycolysis
Myelin Sheath
Electron Transport
Multiple Sclerosis
Cell Survival
Oxidative Stress
Antioxidants
Gene Expression
Proteins

Keywords

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

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Optic nerve degeneration in experimental autoimmune encephalomyelitis. / Guy, John.

In: Ophthalmic Research, Vol. 40, No. 3-4, 01.04.2008, p. 212-216.

Research output: Contribution to journalArticle

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