Cannabinoid-mediated neuroprotection, not immunosuppression, may be more relevant to multiple sclerosis

J. Ludovic Croxford, Gareth Pryce, Samuel J. Jackson, Catherine Ledent, Gavin Giovannoni, Roger G. Pertwee, Takashi Yamamura, David Baker

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

Cannabinoids may exhibit symptom control in multiple sclerosis (MS). We show here that cannabinoid receptor (CBR) agonists can also be immunosuppressive and neuroprotective in models of MS. Immunosuppression was associated with reduced: myelin-specific T cell responses; central nervous system infiltration and reduced clinical disease. This was found to be largely CB1R-dependent and only occurred at doses that induced significant cannabimimetic effects that would not be achieved clinically. Lower, non-immunosuppressive doses of cannabinoids however, slowed the accumulation of nerve loss and disability, despite failing to inhibit relapses. This further highlights the neuroprotective potential of cannabinoids to slow the progression of MS. (C) 2007 Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)120-129
Number of pages10
JournalJournal of Neuroimmunology
Volume193
Issue number1-2
Early online date26 Nov 2007
DOIs
Publication statusPublished - Jan 2008

Keywords

  • cannabinoids
  • experimental autoimmune encephalomyelitis
  • multiple sclerosis
  • immunosuppression
  • neuroprotection
  • placebo-controlled trial
  • CB2 receptor
  • glucocorticoid-receptors
  • endocannabinoid system
  • disease progression
  • interferon-gamma
  • ajulemic acid
  • model
  • agonist

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