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Brain Advance Access originally published online on July 22, 2003
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Brain, Vol. 126, No. 10, 2191-2202, October 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg224

Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

Gareth Pryce*,1, Zubair Ahmed*,1, Deborah J. R. Hankey*,1, Samuel J. Jackson1, J. Ludovic Croxford1, Jennifer M. Pocock1, Catherine Ledent2, Axel Petzold1, Alan J. Thompson3, Gavin Giovannoni1, M. Louise Cuzner1 and David Baker1

1 Department of Neuroinflammation, Institute of Neurology, University College London, London, UK, 2 Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Universite libre de Bruxelles, Brussels, Belgium and 3 Neurorehabilitation Group, Institute of Neurology, University College London, Queen Square, London, UK *These authors contributed equally to this work

Correspondence to: Dr David Baker, Institute of Neurology, University College London, 1 Wakefield Street, London WC1N 1PJ, UK E-mail: d.baker{at}ion.ucl.ac.uk

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.


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