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Huntington's Disease /cannabis Cures

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A preliminary controlled study to determine whether whole plant cannabis extracts can

improve ... Investigating abnormal protein is already promi- nent in neuroscientific research for

neurodegenerative conditions (eg CJD, and Huntington's disease)


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Nabilone Could Treat Chorea and Irritability in Huntington’s Disease

Adrienne Curtis, B.A., B.Sc. and Hugh Rickards, M.D., M.R.C.Psych., Department of Psychiatry, University of Birmingham, Birmingham, United Kingdom



SIR: Huntington’s disease causes chorea and psychiatric abnormalities. Psychiatric symptoms were found in one study in 51 out of 52 patients.1 Dysphoria, agitation, irritability, apathy, and anxiety were found in above 50% of the patients sampled.


Many sources postulate that cannabinoids could have a beneficial effect on the symptoms of Huntington’s disease, especially on choreatic movements.2–4 As well as providing possible symptomatic relief in Huntington’s disease, there is also some evidence5 that cannabinoids might have a neuroprotective effect which could delay the onset of symptoms by delaying or preventing the death of striatal neurons. This neuroprotective effect has also been postulated by other sources.6–8


To date there are only two reports on the use of cannabinoids in Huntington’s disease in the literature. Cannabidiol, a nonpsychotropic cannabinoid, had no effect on chorea severity in 15 patients.9 In one single patient, single dose, uncontrolled open clinical trial using nabilone, 1.5mg, the chorea increased significantly.10 We present a case of a female patient with irritability, which improved after the introduction of cannabis. This improvement was maintained by treatment with nabilone.


Case Report

The patient was a 43-year-old female who died in December 2003. She developed symptoms of Huntington’s disease at the age of 24 and her husband gave up paid employment to care for her in 1990 when she was 30 years old. In 1995, he reported difficulties in caring for his wife. These difficulties were related to personality changes due to her illness. She increasingly resisted help from professionals, especially care assistants, and refused any suggestion of short-term respite care. She became disinhibited and frequently undressed herself and walked around naked inside and occasionally outside the house. She exhibited a number of dangerous behaviors, such as leaving taps running and fires burning, and leaving burning cigarettes around. Her husband became concerned about the effect that the care for his chronically ill wife was having on his son, who was born in 1984.


The patient went into residential care in 1996. The patient’s husband visited two or three times every week and he always took his wife out for a trip. These trips were difficult because of the patient’s refusal to be strapped into the car or her wheelchair, which sometimes resulted in falls caused by violent choreic movements when he was unable to physically hold her in the chair because he was using his hands for some other purpose.


In 2001, he began to give his wife cannabis to smoke when he took her out on these regular trips. When he returned his wife to the nursing home after these visits the staff were aware of a significant difference in the patient. The cannabis appeared to improve her mood and she was calmer and more relaxed. Prior to the introduction of cannabis she was extremely impatient and would get angry if required to wait even a few minutes for a cigarette. After taking cannabis, she was able to wait a while without screaming and throwing things. The patient also willingly accepted the use of a car seat belt and wheelchair harness.


In December 2001, the local general practitioner prescribed a regimen of nabilone, a synthetic 9-keto cannabinoid, which the patient began taking, 1mg each day. The husband and the nursing home staff both reported improvements in behavior and reduction of chorea coinciding with the introduction of cannabis and maintained by daily taking nabilone.



This report has many limitations. It is a single case report and no measurements were taken at the time of the introduction of cannabis and nabilone. The information was obtained by interviewing the husband and staff from the care home in 2005. The symptoms of Huntington’s disease do change over time and the movements are different in the later stages of the disease. However both the husband and the staff are sure that the introduction of cannabis was beneficial and greatly improved the patient’s quality of life in her last years. There is need for further trials to establish the therapeutic use of cannabinoids in the symptomatic treatment of Huntington’s disease.




The first author receives an unrestricted educational grant from Cambridge Laboratories, which holds the European marketing rights for nabilone.





1. Paulsen JS, Ready RE, Hamilton JM, et al: Neuropsychiatric aspects of Huntington’s disease. J Neurol Neurosurg Psychiatry 2001; 71:310–314[Abstract/Free Full Text]

2. Consroe P: Brain cannabinoid systems as targets for the therapy of neurological disorders. Neurobiol Dis 1998; 5:534–551[CrossRef][Medline]

3. Craufurd D, Thompson JC, Snowden JS: Behavioral changes in Huntington disease. Neuropsychiatry Neuropsychol Behav Neurol 2001; 14:219–226[Medline]

4. Goutopoulos A, Makriyannis A: From cannabis to cannabinergics: new therapeutic opportunities. Pharmacol Therapeutics 2002; 95:103–117[CrossRef][Medline]

5. Aiken CT, Tobin AJ, Schweitzer ES: A cell-based screen for drugs to treat Huntington’s disease. Neurobiol Dis 2004; 16:546–555[CrossRef][Medline]

6. Baker D, Pryce G: The therapeutic potential of cannabis in multiple sclerosis. Expert Opin Investig Drugs 2003; 12:561–567[CrossRef][Medline]

7. Croxford JL, Miller SD: Towards cannabis and cannabinoid treatment of multiple sclerosis. Drugs Today 2004; 40:663–676[CrossRef][Medline]

8. Russo E: Future of cannabis and cannabinoids in therapeutics. J Cannabis Therapeutics 2003; 3:163–174

9. Consroe P, Laguna J, Allender J, et al: Controlled clinical trial of cannabidiol in Huntington’s disease. Pharmacol Biochem Behav 1991; 40:701–708[CrossRef][Medline]

10. Muller-Vahl KR, Schneider U, Emrich HMl: Nabilone increases choreatic movements in Huntington’s disease. Mov Disord 1999; 14:1038–1040[CrossRef][Medline]


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Longitudinal Evaluation of Neuropsychiatric Symptoms in Huntington's Disease Jennifer C. Thompson, Ph.D., Jenny Harris, B.Sc., Andrea C. Sollom, M.A., Cheryl L. Stopford, Ph.D., Elizabeth Howard, MBChB, Julie S. Snowden, Ph.D., David Craufurd, M.Sc. The Journal of Neuropsychiatry and Clinical Neurosciences, Jan 2012; 24 (1); 53-60. doi: 10.1176/appi.neuropsych.11030057 /Images/icons/at05_pdf.png PDF





Neurology 36 (Suppl 1) April 1986 p. 342


Reuven Sandyk, Paul Consroe, Lawrence Z. Stern, and Stuart R. Snider, Tucson, AZ




Cannabidiol (CBD) is a major nonpsychoactive cannabinoid of marijuana. Based on reports indicating possible efficacy of CBD in dystonic movements (Neurology 1984; 34 [suppl 1]: 147 and 1985; 35 [suppl 1]: 201), we tried CBD in three patients with Huntington's disease (HD). The patients;, aged 30 to 56, had HD of 7 to 12 years' duration. Their condition has been slowly progressive and unresponsive to prior therapy with neuroleptics. Orally administered CBD was initiated at 300 mg/d and increased 1 week later to 600 mg/d for the next 3 weeks. Mild improvement ( 5 to 15%) in the choreic movements was documented using the tongueprotrusion test (Neurology [Minneap} 1972; 22: 929-33) and a chorea severity evaluation scale (Br J Clin Pharmacol 1981; 11: 129-51) after the first week. Further improvement (20 to 40%) was noticed after the second week of CBD, and this remained stable for the following 2 weeks.


Except for transient, mild hypotension, no side effects were recorded, and laboratory tests were normal. Withdrawal of CBD after 48 hours resulted in return of choreic movements to the pre-CBD state.


(Supported in part by NINCDS grant #NS15441)


source: http://www.druglibrary.org/










Huntington’s disease (HD) is a neurodegenerative autosomal dominant disorder that usually presents in the midlife and is ultimately fatal. The genetic defect affects the IT15 gene located in the short arm of chromosome 4 and that encodes a protein called huntingtin (The Huntington’s Disease Collaborative Group, 1993). The mutation consists of an enlarged repeat of CAG triplets in the 5' coding region, that result in an abnormal polyglutamine tract in the amino-terminal portion of this protein (reviewed by Cattaneo et al., 2005). Normal gene contains between 6 and 35 repeats. Incomplete penetrance was seen for repeats between 36 and 39, whereas the pathology develops with a number of repeats higher than 40 (Landes and Bates, 2004). Mutated huntingtin becomes toxic preferentially for striatal medium-spiny neurons that project to the globus pallidus and the substantia nigra. This produces a progressive degeneration of the striatum that results in a biphasic pattern of motor abnormalities that evolves from an early hyperkinetic phase (choreic movements) to a late akinetic and more disabling phase (reviewed by Walker, 2007). The disease also presents cortical degeneration which originates cognitive dysfuntion and psychiatric symptoms, which are more evident at advanced phases. Despite the fact that the mutated gene responsible for HD has been already identified, the precise molecular and cellular mechanisms underlying striatal degeneration are still unknown and, consequently, the therapeutic outcome for HD patients is still too poor. Several types of compounds are presently under clinical evaluation, including minocycline, coenzyme Q10, unsaturated fatty acids and inhibitors of histone deacetylases (reviewed by Stack and Ferrante, 2007), and a great promise has been concentrated with the case of cannabinoid-based compounds, which have been reported to alleviate motor abnormalities and/or to serve as potential neuroprotective molecules (reviewed by Sagredo et al., 2007).


Cannabinoid-based compounds are a large series of compounds able to target different elements of the so-called cannabinoid system, an intercellular signaling system active in the brain and also in the periphery (reviewed by Mackie and Stella, 2006). This includes selective agonists or antagonists for the CB1 or CB2 receptors, and also for other related receptor types (e.g. TRPV1 receptors), non-selective agonists, and inhibitors of the endocannabinoid generation or inactivation (reviewed by Fowler, 2007). Some of these compounds have been recently examined in animal or cellular models of HD and, although the matter is still far to be completely elucidated, some results have provided promising expectatives for a clinical evaluation in patients (reviewed by Sagredo et al., 2007). Thus, several studies have demonstrated that the loss of CB1 receptor-mediated signaling observed in the basal ganglia of HD patients and animal models (Maccarrone et al., 2007) is a very early event that takes place before the appearance of major neuropathological signs and functional abnormalities, and that it is susceptible of pharmacological correction (Sagredo et al., 2007). In parallel to this progressive decrease experienced by CB1 receptors during the course of this disease, CB2 receptors, whose presence in the healthy striatum is relatively modest, are, however, markedly up-regulated in reactive microglial cells in response to the striatal damage, thus representing a novel target to reduce the toxic influence of these cells on neuronal homeostasis (Fernández-Ruiz et al., 2007). These two observations have served as a basis to explore, at the preclinical level, the potential of both cannabinoid receptor types, and also of other elements of this signaling system in HD. For example, CB1 receptor agonists and inhibitors of the endocannabinoid inactivation have been examined for their possible antihyperkinetic effect, presumably exerted through acutely recovering the neurochemical deficits typical of first grades of this disorder (reviewed by Lastres-Becker et al., 2003). This potential, however, seems to be restricted to certain cannabinoids that combine the capability to enhance the cannabinoid signaling and also to activate TRPV1 receptors (reviewed by Fernández-Ruiz and González, 2005). In addition, cannabinoid agonists can also serve as neuroprotective agents in HD being capable to delay the progression of the striatal degeneration in different experimental models of this disease (reviewed by Sagredo et al., 2007). The neuroprotective effect of cannabinoids would be exerted through three key mechanisms: (i) their capability to normalize glutamate homeostasis, an effect mediated by CB1 receptors, that would allow to reduce excitotoxic events that occur in this pathology (reviewed by Sagredo et al., 2007); (ii) the antioxidant potential of certain cannabinoids, that would be exerted through cannabinoid receptor-independent mechanisms and that would allow to reduce the oxidative injury that also takes place in HD (reviewed by Sagredo et al., 2007); and (iii) their activity at the CB2 receptors to control the microglial influence on neuronal survival, thus reducing the local inflammatory events that are associated with the striatal degeneration (reviewed by Fernández-Ruiz et al., 2007).






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What is Huntington's Disease?









Huntington's disease could be helped through new developments in Scotland involving the medicinal properties of cannabis.


The team of experts at the University of Aberdeen discovered that a naturally-occurring molecule in marijuana - cannabidiol - does not provide the high associated with tetrahydrocannabinol (THC) and as such could be used as an "acceptable drug treatment".


It is believed that many strains of production cannabis are aimed at ramping up the THC content at the expense of cannabidiol, meaning that smoking marijuana could, if anything, exacerbate the problems associated with Huntington's disease and multiple sclerosis.


Dr Bettina Platt, commenting on the findings, said: "We are hoping that our findings can instruct the development of cannabidiol-based treatments for disorders related to mitochondrial dysfunction such as Parkinson's disease or Huntington's disease."


Earlier this month, the NHS reported findings from research in the US published in journal Cancer which linked testicular cancer to the use of cannabis by young males.

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Chemical in Cannabis Helps Cells Grow


Last Updated (Friday, 01 May 2009 14:56) Written by InfoWeb


The fact that cannabis is forbidden in most countries is only a recent event. In the past, starting centuries ago, people always smoked pot for various reasons, including leisure, resting purposes, going into trance, or for medicinal use. In Western societies, it has been mostly forbidden, even though not all of its effects have been fully understood up to this point. This is evidenced by the fact that only recently have researchers managed to identify a substance in cannabis that actually promotes cell growth and helps our bodies function properly.


Out of the 60+ active substances that can be found in the average cannabis or marijuana strain, science has only been able to analyze and assess the threat levels of just a few until now. Yet, there are strict laws in place in every country that forbid the use of the plant, even though you can, for instance, buy flamethrowers in the US, as they pose no danger to anyone.


A team of researchers from the University of Aberdeen describes the roles and functions of cannabidiol, a molecule that is naturally synthesized in the cannabis plant, publishing its finds in the Journal of Neuroscience. It appears that this substance, also known as CBD, has great potential to relieve pain, even though it's not the substance that gives pot its “high” label. Even though physicians have known for quite a long time that the compound can make pains felt by multiple sclerosis patients more bearable, they have never focused on harnessing this power to do good.


Now, UA School of Medical Sciences researcher Dr Bettina Platt, has found out that CBD doesn't actually act on the peripheral nervous system, like other drugs do, but on the brain cells, or neurons themselves, influencing the activity of mitochondria, which are a sort of mini power plants for the cells. Understandably, influencing such an important cellular component into producing more energy is not a bad thing, yet the plant remains illegal because some believe that the other components may indeed be dangerous. However, no one takes the time to actually check them one by one.


“We are hoping that our findings can instruct the development of cannabidiol based treatments for disorders related to mitochondrial dysfunction such as Parkinson's disease or Huntington's disease. There are different strains of cannabis out there and many no longer contain cannabidiol. In fact, these have been deliberately bred out to enhance the THC content,” Platt says, while drawing attention to the fact that smoking cannabis will not necessarily cure these conditions.


In turn, she advocates the extraction of CBD from plants for scientific reasons. It could then be used to synthesize various drugs, which, with some luck, could offer much-needed pain relief for people suffering from some of the worse medical conditions known to man.






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The Synaptic Basis of Learning and Memory in Health and Disease

One of the greatest challenges facing medical science is to defeat neurodegenerative brain disease. As our population ages, more of us will be afflicted by devastating brain disorders such as Alzheimer's disease, Parkinson's disease and senile dementia - neurodegenerative conditions that rob us of the ability to think, to learn and to remember. Until very recently, these diseases remained intractable to modern science. However, rapid advances in molecular genetics and the advent of transgenic models for some of these diseases, has now made it is now possible, for the first time, to study the pathogenic process and examine how it affects the physiology of the brain, especially those mechanisms involved in learning and memory. It is hoped that studies of this type will aid the development of new and effective treatments in the fight against brain disease. The laboratory is interested in how brain disease affects communication between brain cells. In our brains, cells transfer information at specialized structures called synapses. These convert electrical signals into chemical ones that diffuse to the receiving cell where they initiate new electrical signals. Changes in the efficiency of synaptic communication and the connectivity between brain cells are believed to play a vital role in the encoding and storage of information. The most widely studied form of synaptic plasticity thought to be important for learning is that of long-term potentiation (LTP; see ref 1). LTP is an activity-dependent and a lasting increase in the efficiency of transmission at brain synapses; an example is shown on the left. Post-mortern human brain Currently, we are investigating synaptic function in Huntington's disease - a genetic disorder that affects 1-3 people per 20,000 of population.The image shows two sections of human brain, one taken from a normal patient who died of natural causes and one from a patient who died of Huntington's disease. Notice how the Huntington's diseased brain has undergone massive neurodegeneration.


Currently, there is no cure for this devastating condition. Our studies and others show that synaptic plasticity and some aspects of cell function are abnormal in early-stage Huntington's disease (refs 2,3,4). These observations are significant as they occur long before the brain starts to degenerate. If we can identify the cause(s) of these changes we will be able to design new therapies to treat this disease. To this end we are using pharmacological tools to isolate the defective proteins and molecules that give rise to abnormal synaptic plasticity and cell function in Huntington's disease. Inclusions within nuclei of hippocampal neurones.


One possible clue to the pathogenic process involved in Huntington's disease is that, in common with other neurodegenerative diseases, there is an abnormal accumulation of aberrant proteins. In Huntington's disease, these proteins aggregate to form insoluble inclusions that often precipitate within the cell nucleus, disrupting the normal processes of the cell (figure shows inclusions within nuclei of hippocampal neurones; adapted from ref 2). We are examining the relationship between the formation of inclusions and the impairment of synaptic function. In addition, we are also investigating the action of drugs that prevent inclusion formation on synaptic plasticity and cell function.




  1. Bliss TVP and Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361: 31-39.
  2. Murphy KPSJ et al. (2000) Abnormal synaptic plasticity and impaired spatial cognition in mice transgenic for exon 1 of the human Huntington's disease mutation. Journal of Neuroscience 20: 5115-5123.
  3. Hodgson JG et al. (1999) A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration. Neuron 23: 181-192.
  4. Usdin MT et al. (1999) Impaired synaptic plasticity in mice carrying the Huntington's disease mutation. Human Molecular Genetics 8: 839-846.






























Prof Javier Fernández-Ruiz Department of Biochemistry and Molecular Biology and CIBERNED, Faculty of Medicine, Complutense University Archived topic page last updated on 30 July 2008




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At Times, I Really Feel Like I'm Losing It... Great Articles. Well Done BTW.


I Used To Be So Intelligent. Now... It Seems, The Older I Get... The Less I Can Remember.

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