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Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids.
J Neuroimmune Pharmacol. 2015 Jun; 10(2):281-92.JN

Abstract

Multiple sclerosis (MS) is the major immune-mediated, demyelinating, neurodegenerative disease of the central nervous system. Compounds within cannabis, notably Δ9-tetrahydrocannabinol (Δ9-THC) can limit the inappropriate neurotransmissions that cause MS-related problems and medicinal cannabis is now licenced for the treatment of MS symptoms. However, the biology indicates that the endocannabinoid system may offer the potential to control other aspects of disease. Although there is limited evidence that the cannabinoids from cannabis are having significant immunosuppressive activities that will influence relapsing autoimmunity, we and others can experimentally demonstrate that they may limit neurodegeneration that drives progressive disability. Here we show that synthetic cannabidiol can slow down the accumulation of disability from the inflammatory penumbra during relapsing experimental autoimmune encephalomyelitis (EAE) in ABH mice, possibly via blockade of voltage-gated sodium channels. In addition, whilst non-sedating doses of Δ9-THC do not inhibit relapsing autoimmunity, they dose-dependently inhibit the accumulation of disability during EAE. They also appear to slow down clinical progression during MS in humans. Although a 3 year, phase III clinical trial did not detect a beneficial effect of oral Δ9-THC in progressive MS, a planned subgroup analysis of people with less disability who progressed more rapidly, demonstrated a significant slowing of progression by oral Δ9-THC compared to placebo. Whilst this may support the experimental and biological evidence for a neuroprotective effect by the endocannabinoid system in MS, it remains to be established whether this will be formally demonstrated in further trials of Δ9-THC/cannabis in progressive MS.

Authors+Show Affiliations

Neuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, E1 2AT, UK, g.pryce@qmul.ac.uk.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

25537576

Citation

Pryce, Gareth, et al. "Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis By Cannabis-Based Cannabinoids." Journal of Neuroimmune Pharmacology : the Official Journal of the Society On NeuroImmune Pharmacology, vol. 10, no. 2, 2015, pp. 281-92.
Pryce G, Riddall DR, Selwood DL, et al. Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids. J Neuroimmune Pharmacol. 2015;10(2):281-92.
Pryce, G., Riddall, D. R., Selwood, D. L., Giovannoni, G., & Baker, D. (2015). Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids. Journal of Neuroimmune Pharmacology : the Official Journal of the Society On NeuroImmune Pharmacology, 10(2), 281-92. https://doi.org/10.1007/s11481-014-9575-8
Pryce G, et al. Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis By Cannabis-Based Cannabinoids. J Neuroimmune Pharmacol. 2015;10(2):281-92. PubMed PMID: 25537576.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids. AU - Pryce,Gareth, AU - Riddall,Dieter R, AU - Selwood,David L, AU - Giovannoni,Gavin, AU - Baker,David, Y1 - 2014/12/24/ PY - 2014/10/26/received PY - 2014/12/10/accepted PY - 2014/12/25/entrez PY - 2014/12/30/pubmed PY - 2016/4/2/medline SP - 281 EP - 92 JF - Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology JO - J Neuroimmune Pharmacol VL - 10 IS - 2 N2 - Multiple sclerosis (MS) is the major immune-mediated, demyelinating, neurodegenerative disease of the central nervous system. Compounds within cannabis, notably Δ9-tetrahydrocannabinol (Δ9-THC) can limit the inappropriate neurotransmissions that cause MS-related problems and medicinal cannabis is now licenced for the treatment of MS symptoms. However, the biology indicates that the endocannabinoid system may offer the potential to control other aspects of disease. Although there is limited evidence that the cannabinoids from cannabis are having significant immunosuppressive activities that will influence relapsing autoimmunity, we and others can experimentally demonstrate that they may limit neurodegeneration that drives progressive disability. Here we show that synthetic cannabidiol can slow down the accumulation of disability from the inflammatory penumbra during relapsing experimental autoimmune encephalomyelitis (EAE) in ABH mice, possibly via blockade of voltage-gated sodium channels. In addition, whilst non-sedating doses of Δ9-THC do not inhibit relapsing autoimmunity, they dose-dependently inhibit the accumulation of disability during EAE. They also appear to slow down clinical progression during MS in humans. Although a 3 year, phase III clinical trial did not detect a beneficial effect of oral Δ9-THC in progressive MS, a planned subgroup analysis of people with less disability who progressed more rapidly, demonstrated a significant slowing of progression by oral Δ9-THC compared to placebo. Whilst this may support the experimental and biological evidence for a neuroprotective effect by the endocannabinoid system in MS, it remains to be established whether this will be formally demonstrated in further trials of Δ9-THC/cannabis in progressive MS. SN - 1557-1904 UR - https://www.unboundmedicine.com/medline/citation/25537576/Neuroprotection_in_Experimental_Autoimmune_Encephalomyelitis_and_Progressive_Multiple_Sclerosis_by_Cannabis_Based_Cannabinoids_ L2 - https://doi.org/10.1007/s11481-014-9575-8 DB - PRIME DP - Unbound Medicine ER -