Phytochemicals and Cannabinoids from Cannabis Spp. implicated in the treatment of Multiple Sclerosis

Multiple sclerosis is an inflammatory disease that causes demyelination of nerve cells in the central nervous system resulting in muscle weakness, spasticity and loss of motor coordination.

CB1 receptors have been shown to regulate synaptic neurotransmission leading to control of spasticity.  CB2 receptors which are expressed in microglial cells (the main form of immune defence in the brain and spinal cord) may be upregulated in inflammation of brain tissue. Evidence shows that CB2 receptors plays a major role in autoimmune CNS inflammation.

Studies using experimental autoimmune encephalomyelitis (EAE) to induce MS conditions in revealed reduced endocannabinoid levels in in the cerebrospinal fluid (CSF) relative to controlled subjects. Several studies have also shown that THC is effective and well tolerated in reducing muscle spasticity and there were no major safety concerns with THC over a twelve month period in its administration to MS patients.


Three phytocannabinoids have been implicated in the management and treatment of multiple sclerosis. They are:

  • Tetrahydrocannabinol (THC): HU-210, a THC analogue reduced excitotoxicity of axonal neurons due to activation of CB1 and CB2 receptors.  This resulted in a decrease in the excitability of the neurons and a control of muscle spasticity.
  • Cannabidiol (CBD): In an EAE model of multiple sclerosis in mice, CBD reduced damage to axonal neurons and reduced inflammation and activation of microglial T-cell recruitment in the spinal cord. •    CBD also suppresses immune responses such as release of cytokines, chemokines, growth factors, as well as immune cell proliferation, activation, maturation, migration and antigen presentation. Cannabidiol has thereby proven to be immunosuppressive, anti-oxidant and neuroprotective, making it a powerful agent in the inflammatory processes involved in multiple sclerosis.
  • Cannabigerol (CBG): CBG has resulted in decreased microglial activity in an MS model. It has also shown protection against excitotoxicity, thereby preventing neuronal cell death.

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