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Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

Gareth Pryce, Zubair Ahmed, Deborah J. R. Hankey, Samuel J. Jackson, J. Ludovic Croxford, Jennifer M. Pocock, Catherine Ledent, Axel Petzold, Alan J. Thompson, Gavin Giovannoni, M. Louise Cuzner, David Baker
DOI: http://dx.doi.org/10.1093/brain/awg224 2191-2202 First published online: 22 July 2003

Summary

Multiple sclerosis is increasingly being recognized as a neurodegenerative disease that is triggered by inflammatory attack of the CNS. As yet there is no satisfactory treatment. Using experimental allergic encephalo myelitis (EAE), an animal model of multiple sclerosis, we demonstrate that the cannabinoid system is neuroprotective during EAE. Mice deficient in the cannabinoid receptor CB1 tolerate inflammatory and excito toxic insults poorly and develop substantial neurodegeneration following immune attack in EAE. In addition, exogenous CB1 agonists can provide significant neuroprotection from the consequences of inflammatory CNS disease in an experimental allergic uveitis model. Therefore, in addition to symptom management, cannabis may also slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis and probably other diseases.

  • Keywords: cannabinoids; excitotoxicity; experimental allergic encephalomyelitis; multiple sclerosis; neuroprotection
  • Abbreviations: 2‐AG = 2‐arachidonoyl glycerol; CB = cannabinoid receptor; CREAE = chronic relapsing experimental allergic encephalomyelitis; EAE = experimental allergic encephalomyelitis; EAU = experimental allergic uveitis; ELISA = enzyme‐linked immunosorbent assay; i.p. = intraperitoneal; IRBP = interphotoreceptor retinoid binding protein; NMDA = N‐methyl‐d‐aspartate; Δ9‐THC = tetrahydrocannabinol
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