LINGO-1 and AMIGO3, potential therapeutic targets for neurological and dysmyelinating disorders?

Simon Foale, Martin Berry, Ann Logan, Daniel Fulton, Zubair Ahmed

Research output: Contribution to journalReview articlepeer-review

6 Citations (Scopus)
286 Downloads (Pure)


Leucine rich repeat proteins have gained considerable interest as therapeutic targets due to their expression and biological activity within the central nervous system. LINGO-1 has received particular attention since it inhibits axonal regeneration after spinal cord injury in a RhoA dependent manner while inhibiting leucine rich repeat and immunoglobulin-like domain-containing protein 1 (LINGO-1) disinhibits neuron outgrowth. Furthermore, LINGO-1 suppresses oligodendrocyte precursor cell maturation and myelin production. Inhibiting the action of LINGO-1 encourages remyelination bothin vitroandin vivo. Accordingly, LINGO-1 antagonists show promise as therapies for demyelinating diseases. An analogous protein to LINGO-1, amphoterin-induced gene and open reading frame-3 (AMIGO3), exerts the same inhibitory effect on the axonal outgrowth of central nervous system neurons, as well as interacting with the same receptors as LINGO-1. However, AMIGO3 is upregulated more rapidly after spinal cord injury than LINGO-1. We speculate that AMIGO3 has a similar inhibitory effect on oligodendrocyte precursor cell maturation and myelin production as with axogenesis. Therefore, inhibiting AMIGO3 will likely encourage central nervous system axonal regeneration as well as the production of myelin from local oligodendrocyte precursor cell, thus providing a promising therapeutic target and an area for future investigation.

Original languageEnglish
Pages (from-to)1247-1251
Number of pages5
JournalNeural Regeneration Research
Issue number8
Publication statusPublished - 5 Sept 2017


  • Journal Article
  • Review
  • multiple sclerosis
  • demyelination
  • oligodendrocyte
  • AMIGO3
  • LINGO1
  • oligodendrocyte precursor cell


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