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Overview of Huntington's Disease

Huntington’s disease is an inherited progressive degenerative disease that causes nerve cells in the basal ganglia of the brain to waste away. The disease, also commonly referred to as HD or Huntington’s chorea, causes psychiatric disorders and affects a person’s movement and cognitive abilities. People with Huntington’s disease are born with the defective gene, as there’s a 50 percent chance of getting it if one parent has the disease, according to the National Institute of Neurological Disorders and Stroke. However, symptoms most commonly don’t develop until middle age.

Movement-related symptoms of Huntington’s disease typically begin with uncontrolled movements, balance problems, and overall clumsiness. Patients can experience dystonia, involuntary jerking movements, and impaired gait and posture. Eventually, the disease can take away the ability to walk, talk, and swallow. Cognitive impairments commonly associated with the disease can include a difficulty organizing, prioritizing, and focusing on tasks, a tendency to get stuck on a thought or action, difficulty learning new information, and a lack of impulse control. The most common psychiatric disorder caused by Huntington’s disease is depression, but the disease can also lead to insomnia, fatigue and loss of energy, social withdrawal, and feelings of irritability, sadness, and apathy.

Functional, cognitive, and psychiatric health worsens over time after the onset of Huntington’s disease. The rate of disease progression and duration varies, but eventually a person requires daily living help. There is no cure for the disorder, but some medications can help manage symptoms. Additionally, physical, occupational, speech, and psychotherapies can help patients address movement, behavioral, and psychiatric problems.

Findings: Effects of Cannabis on Huntington's Disease

Research has shown that cannabis helps slow the progression of Huntington’s disease through its interaction with the endocannabinoid system. After studies determined that Huntington’s disease was related to a loss of cannabinoid receptors in the basal ganglia, researchers set out to examine whether increasing endocannabinoid activity could be therapeutically beneficial for treating the disease1. Results have been encouraging.

In preclinical trials, the major cannabinoids found in cannabis, tetrahydrocannabinol (THC) and cannabidiol (CBD) have been found to be effective at protecting the life of neurons in the brain. Research has shown that through the activation of cannabinoid 2 receptors (CB2), the inflammation and toxicity of microglial cells is reduced, which in turn slows the neurodegeneration caused by Huntington’s disease3,4,10. Through the activation of cannabinoid 1 receptors (CB1), cannabinoids have shown to effectively alleviate specific motor symptoms like tremors and movement disorders and reduce the process in which neurons are damaged and killed to slow the progression of the disease1,2,12.

Additionally, studies examining the effect of cannabis-based medications on Huntington’s disease have proven cannabinoids effective at delaying the progression of the disorder7,11,13,14,15.

Researchers have concluded that targeting the cannabinoid system with cannabinoids has a potential therapeutic benefit for treating basal ganglia disorders like Parkinson’s disease and Huntington’s disease2. The cannabinoids are effective at providing neuroprotection through three methods: reducing inflammation by activating CB2 receptors, limiting cell death by activating CB1 receptors, and providing an antioxidant effect through a mechanism independent of cannabinoid receptors9,11. Studies also indicate that cannabinoids are effective at reducing muscle spasms and the inability to concentrate through their direct activation of vanilloid TRPV(1) receptors9.


  1. Dowie, M.J., Bradshaw, H.B., Howard, M.L., Nicholson, L.F., Faull, R.L., Hannan, A.J., and Glass, M. (2009, September). Altered CB1 receptor and endocannabinoid levels precede motor symptom onset in a transgenic mouse model of Huntington’s disease. Neuroscience, 163(1), 456-65. Retrieved from

  2. Fernández-Ruiz, J. (2009). The endocannabinoid system as a target for the treatment of motor dysfunction. British Journal of Pharmacology, 156(7), 1029–1040. Retrieved from

  3. Fernández-Ruiz, J., Pazos, M.R., García-Arencibia, M., Sagredo, O., and Ramos, J.A. (2008, April). Role of CB2 receptors in neuroprotective effects of cannabinoids. Molecular and Cellular Endocrinology, 286(1-2 Suppl 1): S91-6. Retrieved from

  4. Fernández-Ruiz, J., Moreno-Martet, M., Rodríguez-Cueto, C., Palomo-Garo, C., Gómez-Cañas, M., Valdeolivas, S., Guaza, C., Romero, J., Guzman, M., Mechoulam, R., and Ramos, J. A. (2011). Prospects for cannabinoid therapies in basal ganglia disorders. British Journal of Pharmacology, 163(7), 1365–1378. Retrieved from

  5. Huntington’s Disease. (2016, February 24). MedlinePlus. Retrieved from

  6. Huntington’s disease. (2014, July 24). Mayo Clinic. Retrieved from

  7. Iuvone, T., Esposito, G., De Filippis, D., Scuderi, C., and Steardo, L. (2009, Winter). Cannabidiol: a promising drug for neurodegenerative disorders? CNS Neuroscience & Therapeutics, 15(1), 65-75. Retrieved from

  8. Latres-Becker, I., Hansen, H.H., Berrendero, F., De Miguel, R., Pérez-Rosado, A., Manzanares, J., Ramos, J.A., and Fernández-Ruiz, J. (2002, April). Alleviation of motor hyperactivity and neurochemical deficits by endocannabinoid uptake inhibition in a rat model of Huntington’s disease. Synapse, 44(1), 23-35. Retrieved from

  9. Pazos, M.R., Sagredo, O., and Fernández-Ruiz, J. (2008). The endocannabinoid system in Huntington’s disease. Current Pharmaceutical Design, 14(23), 2317-25. Retrieved from

  10. Sagredo, O., Ramos, J.A., Decio, A., Mechoulam, R., and Fernández-Ruiz, J. (2007, August). Cannabidiol reduced the striatal atrophy caused 3-nitropropionic acid in vivo by mechanisms independent of the activation of cannabinoid, vanilloid TRPV1 and adenosine A2A receptors. The European Journal of Neuroscience, 26(4), 843-51. Retrieved from

  11. Sagredo, O., García-Arencibia, M., de Lago, E., Finetti, S., Decio, A., and Fernández-Ruiz, J. (2007, August). Cannabinoids and neuroprotection in basal ganglia disorders. Molecular Neurobiology, 36(1), 82-91. Retrieved from

  12. Sagredo, O., González, S., Aroyo, I., Pazos, M. R., Benito, C., Lastres-Becker, I., Romero, J.P., tolon, R.M., Mechoulam, R., Brouillet, E., Romero, J., and Fernández-Ruiz, J. (2009). Cannabinoid CB2 receptor agonists protect the striatum against malonate toxicity: relevance for Huntington’s disease. Glia, 57(11), 1154–1167. Retrieved from

  13. Sagredo, O., Pazos, M.R., Satta, V., Ramos, J.A., Pertwee, R.G., and Fernández-Ruiz, J. (2011, September). Neuroprotective effects of phytocannabinoid-based medicines in experimental models of Huntington’s disease. Journal of Neuroscience Research, 89(9), 1509-18. Retrieved from

  14. Sagredo, O., Pazos, M.R., Valdeolivas, S., and Fernández-Ruiz, J. (2012, April). Cannabinoids: novel medicines for the treatment of Huntington’s disease. Recent Patents on CNS Drug Discovery, 7(1), 41-8. Retrieved from

  15. Valdeolivas, S., Satta, V., Pertwee, R. G., Fernández-Ruiz, J., and Sagredo, O. (2012). Sativex-like Combination of Phytocannabinoids is Neuroprotective in Malonate-Lesioned Rats, an Inflammatory Model of Huntington’s Disease: Role of CB1 and CB2 Receptors. ACS Chemical Neuroscience, 3(5), 400–406. Retrieved from

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