Cannabis could hold the key to ending
multiple sclerosis misery
multiple sclerosis misery
Researchers investigating the role of cannabinoids - chemical substances contained within cannabis
in the treatment of multiple sclerosis (MS), have found they could significantly enhance therapy, not
only by reducing nerve damage and erratic nerve impulses, but perhaps even by hindering
development of the condition.
in the treatment of multiple sclerosis (MS), have found they could significantly enhance therapy, not
only by reducing nerve damage and erratic nerve impulses, but perhaps even by hindering
development of the condition.
The findings, published online today (1 April, 2007) in
Nature Medicine demonstrates for the first time how
cannabis might actually slow down the progression of MS and could have major implications for the
estimated 2.5 million sufferers worldwide.
Using a mouse model, a team of UK, European, Japanese and US scientists, led by David Baker, Professor
of Neuroimmunology at Queen Mary, University of London, found that doses of the active component
within cannabis, tetrahydrocannabinol (THC) could significantly inhibit the development and severity of
MS.
Cannabis works because it stimulates molecules known as cannabinoid receptors within the body. The
group had previously reported that THC could alleviate disease symptoms, and also save nerves from the
damaging effects of the disease - thus potentially, via the cannabinoid receptor CB1, slowing down the
development of progressive disability. They had not previously examined the influence of cannabinoids on
immune aspects of the disease.
Now their most recent study has successfully separated the roles of cannabinoid receptors CB1 and CB2 on
neurons and T cells, and investigated their effect in controlling central nervous system autoimmunity. It
showed that CB1 receptor expression by nerves in the brain, but not T cells, could suppress the
development of an experimental MS-like disease, by stimulating the release of anti-inflammatory
molecules, whilst in contrast direct stimulation of CB2 receptors by T cells was also able to control
inflammation associated with the condition. This suggests that cannabis-like drugs may have the potential
to block the autoimmune response which drives disease development.
Professor David Baker said: Whilst targeting CB1 receptors for therapy runs the risk of causing the
unwanted high to achieve these effects, we can get the same result by targeting CB2 receptors, which
avoids these risks. Therefore, we can start to think about using new drugs that harness the potential medical
benefits that cannabis has to offer but move away from the issues over the legality and recreational use of
the plant product.
Source: Queen Mary, University of London
cannabis might actually slow down the progression of MS and could have major implications for the
estimated 2.5 million sufferers worldwide.
Using a mouse model, a team of UK, European, Japanese and US scientists, led by David Baker, Professor
of Neuroimmunology at Queen Mary, University of London, found that doses of the active component
within cannabis, tetrahydrocannabinol (THC) could significantly inhibit the development and severity of
MS.
Cannabis works because it stimulates molecules known as cannabinoid receptors within the body. The
group had previously reported that THC could alleviate disease symptoms, and also save nerves from the
damaging effects of the disease - thus potentially, via the cannabinoid receptor CB1, slowing down the
development of progressive disability. They had not previously examined the influence of cannabinoids on
immune aspects of the disease.
Now their most recent study has successfully separated the roles of cannabinoid receptors CB1 and CB2 on
neurons and T cells, and investigated their effect in controlling central nervous system autoimmunity. It
showed that CB1 receptor expression by nerves in the brain, but not T cells, could suppress the
development of an experimental MS-like disease, by stimulating the release of anti-inflammatory
molecules, whilst in contrast direct stimulation of CB2 receptors by T cells was also able to control
inflammation associated with the condition. This suggests that cannabis-like drugs may have the potential
to block the autoimmune response which drives disease development.
Professor David Baker said: Whilst targeting CB1 receptors for therapy runs the risk of causing the
unwanted high to achieve these effects, we can get the same result by targeting CB2 receptors, which
avoids these risks. Therefore, we can start to think about using new drugs that harness the potential medical
benefits that cannabis has to offer but move away from the issues over the legality and recreational use of
the plant product.
Source: Queen Mary, University of London
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