Steps in Multiple Sclerosis Pathogenesis - II: The Role of Biological Markers, Sodium Channels and Glutamate in Neurodegeneration

Aydin O. F., Kurne A., Karabudak R.

TURKISH JOURNAL OF NEUROLOGY, vol.12, no.2, pp.98-105, 2006 (ESCI) identifier

  • Publication Type: Article / Review
  • Volume: 12 Issue: 2
  • Publication Date: 2006
  • Journal Name: TURKISH JOURNAL OF NEUROLOGY
  • Journal Indexes: Emerging Sources Citation Index (ESCI), TR DİZİN (ULAKBİM)
  • Page Numbers: pp.98-105
  • Keywords: multiple sclerosis, immunopathogenesis, neurodegeneration
  • Ondokuz Mayıs University Affiliated: Yes

Abstract

Scientific background: Neurodegeneration following inflammatory injury is considered to be a pathological correlate of irreversible disability in patients with multiple sclerosis (MS). The presence of amyloid precursor protein in active lesions, oxidative injury of mitochondrial DNA, dis/inactivation of mitochondrial enzymes, loss of axonal density in normal appearing white matter, reduction of N-acetylaspartate (NAA)/creatinin ratio in magnetic resonance spectroscopy (MRS) and the correlation between reduced NAA levels and disability have been determined as evidences of neurodegeneration in MS. In the disease immunopathogenesis some biological indicators of axonal transsection as NAA, actin, tubulin, L-neurofilaments, anti-axolemma IgG, antigangliozide antibodies, glial fibrillary acid protein, S-100 protein, nitric oxide, neuronal specific enolase, 14-3-3 protein, apoprotein E have been described and put in association with the clinicial status.