Axonal degeneration in multiple sclerosis: defining therapeutic targets by identifying the causes of pathology

Jae Young Lee, Melissa Biemond, Steven Petratos

Research output: Contribution to journalReview ArticleResearchpeer-review

10 Citations (Scopus)


Current therapeutics in multiple sclerosis (MS) target the putative inflammation and immune attack on CNS myelin. Despite their effectiveness in blunting the relapse rate in MS patients, such therapeutics do not prevent MS disease progression. Importantly, specific clinical dilemma arises through inability to predict MS progression and thereby therapeutically target axonal injury during MS, limiting permanent disability. The current review identifies immune and neurobiological principles that govern the sequelae of axonal degeneration during MS disease progression. Defining the specific disease arbiters, inflammatory and autoimmune, oligodendrocyte dystrophy and degenerative myelin, we discuss a basis for a molecular mechanism in axons that may be targeted therapeutically, in spatial and temporal manner to limit axonal degeneration and thereby halt progression of MS.

Original languageEnglish
Pages (from-to)527-548
Number of pages22
JournalNeurodegenerative Disease Management
Issue number6
Publication statusPublished - 1 Dec 2015


  • axo-glial unit
  • axonal degeneration
  • CD8 T cells
  • experimental autoimmune encephalomyelitis
  • myelin debris
  • Nogo receptor 1
  • NogoA
  • oligodendrocyte dystrophy
  • progressive multiple sclerosis
  • Th17 T cells

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