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Seeking Help To Include Parkinson's As Qualifying Condition


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• These findings indicate a link between endocannabinoid signaling and symptoms of Parkinson’s disease, and suggest that modulation of the endocannabinoid signaling system might prove useful in treating this or other basal ganglia-related movement disorders.

http://www.fasebj.org/content/14/10/1432.full

 

 

• Long-term treatment with levodopa in Parkinson's disease results in the development of motor fluctuations, including reduced duration of antiparkinsonian action and involuntary movements, i.e., levodopa-induced dyskinesia. We tested the hypothesis that the cannabinoid receptor agonist would alleviate levodopa-induced dyskinesia in Parkinson's disease. There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of cannabinoid agonist increased the duration of antiparkinsonian action of levodopa by 76%. Thus, cannabinoid receptor agonists may be useful in the treatment of motor complications in Parkinson's disease.

http://onlinelibrary.wiley.com/doi/10.1002/mds.10289/abstract;jsessionid=1895E9744674D12E8E3FE0928973B1E2.f01t01?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

 

• In recent years, an increased understanding of the physiological role of transmission at CB1 receptors throughout the basal ganglia circuitry has led to the identification of novel therapeutic approaches to both the symptoms of Parkinson’s disease and the side effects of current anti-parkinsonian therapies

http://www.sciencedirect.com/science/article/pii/S1471489202000115

 

 

• We have recently demonstrated that two plant-derived cannabinoids, Δ9-tetrahydrocannabinol and cannabidiol (CBD), are neuroprotective in an animal model of Parkinson's disease (PD). Our results indicate that those cannabinoids having antioxidant cannabinoid receptor-independent properties provide neuroprotection against the progressive degeneration of nigrostriatal dopaminergic neurons occurring in PD.

http://www.sciencedirect.com/science/article/pii/S0006899306034718

 

• In summary, our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD.

http://www.sciencedirect.com/science/article/pii/S0969996104002827

 

• The data suggest that both CB1 cannabinoid receptor antagonists and agonists can modulate the behavioural effects of L-dopa and may be useful for the treatment of the dyskinesia associated with long-term L-dopa treatment of Parkinson's disease.

http://onlinelibrary.wiley.com/doi/10.1002/mds.10312/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

• Levodopa is the most commonly prescribed drug for Parkinson's disease (PD). Although levodopa improves PD symptoms in the initial stages of the disease, its long-term use is limited by development of side effects, including abnormal involuntary movements (dyskinesias) and psychiatric complications. The endocannabinoid system is emerging as an important modulator of basal ganglia functions and its pharmacologic manipulation represents a promising therapy to alleviate levodopa-induced dyskinesias.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2128772/

 

• The management of psychosis in Parkinson’s disease (PD) has been considered a great challenge for clinicians and there is a need for new pharmacological intervention. Previously an antipsychotic and neuroprotective effect of Cannabidiol (CBD) has been suggested. Therefore, the aim of the present study was to directly evaluate for the first time, the efficacy, tolerability and safety of CBD on PD patients with psychotic symptoms. This was an open-label pilot study. The psychotic symptoms evaluated by the Brief Psychiatric Rating Scale and the Parkinson Psychosis Questionnaire showed a significant decrease under CBD treatment. CBD did not worsen the motor function and decreased the total scores of the Unified Parkinson’s Disease Rating Scale. No adverse effect was observed during the treatment. These preliminary data suggest that CBD may be effective, safe and well tolerated for the treatment of the psychosis in PD.

http://jop.sagepub.com/content/23/8/979.short

 

• In recent years, new data support the idea of a relevant role for the cannabinoid system in PD. As cannabinoids have neuroprotective properties, they have been proposed as potentially useful neuroprotective substances in PD, as well as to alleviate some symptoms in specific circumstances (i.e. parkinsonian tremor associated with overactivity to the subthalamic nucleus; levodopainduced dyskinesia). By contrast, CB1 receptor antagonists might be useful to reduce bradykinesia in patients refractory to classic levodopa treatment. Collectively, all these evidence support that the management of the cannabinoid system might represent a new approach to the treatment of PD.

http://www.ingentaconnect.com/content/ben/cmc/2006/00000013/00000030/art00007

 

• An anonymous questionnaire sent to all patients attending the Prague Movement Disorder Centre revealed that 25% of 339 respondents had taken cannabis and 45.9% of these described some form of benefit.

http://onlinelibrary.wiley.com/doi/10.1002/mds.20111/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

• There is evidence that cannabinoid-based medicines that are selective for different targets in the cannabinoid signalling system might be beneficial in basal ganglia disorders, namely Parkinson's disease (PD) and Huntington's disease (HD). These benefits not only include the alleviation of specific motor symptoms, but also the delay of disease progression due to the neuroprotective properties demonstrated for cannabinoids.

http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2008.00088.x/full

 

 

 

 

 

• The CB system is emerging as a key regulator of neuronal cell fate and is capable of conferring neuroprotection by the direct engagement of prosurvival pathways and the control of neurogenesis. Many neurological conditions feature a neurodegenerative component that is associated with excitotoxicity, oxidative stress, and neuroinflammation, and certain CB molecules have been demonstrated to inhibit these events to halt the progression of neurodegeneration.

http://onlinelibrary.wiley.com/doi/10.1111/j.1755-5949.2010.00195.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

• Cannabinoid-based medicines have been proposed as clinically promising therapies in Parkinson's disease (PD), given the prominent modulatory function played by the cannabinoid signaling system in the basal ganglia. Supporting this pharmacological potential, the cannabinoid signaling system experiences a biphasic pattern of changes during the progression of PD. This would explain the motor inhibition typical of this disease and the potential proposed for CB1 receptor antagonists in attenuating the bradykinesia typical of PD. In addition, certain cannabinoid agonists have been proposed to serve as neuroprotective molecules in PD, given their well-demonstrated capability to reduce excitotoxicity, calcium influx, glial activation and, in particular, oxidative injury that cooperatively contribute to the degeneration of nigral neurons.

http://www.ingentaconnect.com/content/ben/cnsnddt/2009/00000008/00000006/art00004

 

• The co-expression of cannabinoid and dopamine receptors in the basal ganglia suggests a potential role for endocannabinoids in the control of voluntary movement in Parkinson's disease. Our results indicate that activation of the CB1 stimulates the dopaminergic system ipsilaterally to the lesion, and may have implications in the treatment of Parkinson's disease.

http://onlinelibrary.wiley.com/doi/10.1034/j.1600-0773.2003.930202.x/full

 

• The last five years have shown a remarkable increase in publications on cannabidiol mainly stimulated by the discovery of its anti-inflammatory, anti-oxidative and neuroprotective effects. These studies have suggested a wide range of possible therapeutic effects of cannabidiol on several conditions, including Parkinson's disease, Alzheimer's disease, cerebral ischemia, diabetes, rheumatoid arthritis, other inflammatory diseases, nausea and cancer.

http://www.scielo.br/scielo.php?pid=S1516-44462008000300015&script=sci_arttext

 

• Cannabidiol (CBD) was given to 5 patients with dystonic movement disorders in a preliminary open pilot study. Oral doses of CBD rising from 100 to 600 mg/day over a 6 week period were administered along with standard medication. Dose-related improvement in dystonia was observed in all patients and ranged from 20 to 50%. CBD appears to have antidystonic and Parkinsonism-aggravating effects in humans.

 

http://informahealthcare.com/doi/abs/10.3109/00207458608985678

 

• The neuroprotective potential of CBD, based on the combination of its anti-inflammatory and anti-oxidant properties, is of particular interest and is presently under intense preclinical research in numerous neurodegenerative disorders. In fact, CBD combined with Δ9-tetrahydrocannabinol is already under clinical evaluation in patients with Huntington's disease to determine its potential as a disease-modifying therapy.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2012.04341.x/full

 

• Cannabinoids derived from Cannabis sativa demonstrate neuroprotective properties in various cellular and animal models. Mitochondrial impairment and consecutive oxidative stress appear to be major molecular mechanisms of neurodegeneration. Therefore we studied some major cannabinoids, i.e. delta-9-tetrahydrocannabinolic acid (THCA), delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) in a Parkinson's disease model. Our data show that cannabinoids THC and THCA protect dopaminergic neurons against MPP+ induced cell death.

http://www.sciencedirect.com/science/article/pii/S0944711312001249

 

• This review discusses recent studies suggesting that cannabidiol may have utility in treating a number of human diseases and disorders now known to involve activation of the immune system and associated oxidative stress, as a contributor to their etiology and progression. This includes Parkinson's disease.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085542/

 

• Cannabidiol (CBD) is a non-psychotomimetic compound from Cannabis sativa plant that produces antipsychotic effects in rodents and humans. It also reverses L-dopa-induced psychotic symptoms and improves motor function in Parkinson's patients.

http://www.sciencedirect.com/science/article/pii/S0278584613001164

 

• We have previously shown a protective effect of Δ9-tetrahydrocannabinol (THC) in Parkinson's disease (PD) cell culture models associated with increased CB1 cannabis receptor cDNA. Our results suggest that the protective effects of cannabinoids in cell culture models of PD may be mediated by modulation of the ECS.

http://jnnp.bmj.com/content/81/11/e60.1.short

 

• It seems that cannabinoids could delay or even stop progressive degeneration of brain dopaminergic systems, a process for which there is presently no prevention. In combination with currently used drugs, cannabinoids might represent, qualitatively, a new approach to the treatment of PD, making it more effective.

http://link.springer.com/article/10.2165/00002512-200016060-00001

 

• We have demonstrated up-regulation of the CB1 receptor in direct response to neuronal injury in a human PD cell culture model, and a direct neuronal protective effect of Δ9-THC that may be mediated through PPARγ activation.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2990.2011.01248.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

• Given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Δ9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for ameliorating parkinsonian symptoms.

http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2011.01278.x/full

 

• Marijuana works for Parkinson's disease and many patients are coming forward and describing the relief they get from it. Prohibition has been wrong especially for those with medical needs.

http://books.google.com/books?hl=en&lr=&id=OF9LJas-MJAC&oi=fnd&pg=PT5&dq=parkinson%27s+thcv&ots=-H9Kkk7qAD&sig=t9P7BbYbZRh7UXubo1l_dhJH-hI#v=onepage&q&f=false

 

 

 

 

 

• CBD has also been found to be highly effective as a neuroprotective compound in experimental models of parkinsonism. There could well be clinical advantages to administering Δ9-THCV together with CBD as this might induce symptomatic relief (due to the blockade of CB1 by Δ9-THCV) and neuroprotection (due to the anti-oxidant and anti-inflammatory properties of both CBD and Δ9-THCV). The combination of CBD with Δ9-THCV would merit investigation in parkinsonian patients.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2012.04341.x/full

 

• In an increasingly ageing population, the incidence of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Huntington's disease are rising. While the aetiologies of these disorders are different, a number of common mechanisms that underlie their neurodegenerative components have been elucidated; namely neuroinflammation, excitotoxicity, mitochondrial dysfunction and reduced trophic support. Current therapies focus on treatment of the symptoms and attempt to delay the progression of these diseases but there is currently no cure. Modulation of the endogenous cannabinoid system is emerging as a potentially viable option in the treatment of neurodegeneration. Endocannabinoid signalling has been found to be altered in many neurodegenerative disorders. To this end, pharmacological manipulation of the endogenous cannabinoid system, as well as application of phytocannabinoids and synthetic cannabinoids have been investigated. Through multiple lines of evidence, this evolutionarily conserved neurosignalling system has shown neuroprotective capabilities and is therefore a potential target for neurodegenerative disorders. This review details the mechanisms of neurodegeneration and highlights the beneficial effects of cannabinoid treatment.

http://onlinelibrary.wiley.com/doi/10.1111/bph.12492/abstract

 

• Emerging evidence highlights the beneficial effects of the whole cannabis extract over those observed with single components.

http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200790146/abstract

 

• The invention relates to the use of cannabinoid-containing plant extracts in the prevention or treatment of neural degeneration. In particular, the invention relates to use of one or more cannabinoid-containing plant extracts in the prevention or treatment of neural degeneration (such as Parkinson's disease).

http://www.google.com/patents/US20100239693

 

• Parkinson’s disease (PD) is a neurodegenerative disorder caused by a progressive loss of dopaminergic neurons of the substantia nigra, resulting from an oxidative stress. The lack of dopaminergic neurons is reflected by a disturbed balance of the neural circuitry in the basal ganglia. Cannabinoids might alleviate some parkinsonian symptoms by their remarkable receptor-mediated modulatory action in the basal ganglia output nuclei. Moreover, it was recently observed that some cannabinoids are potent antioxidants that can protect neurons from death even without cannabinoid receptor activation. It seems that cannabinoids could delay or even stop progressive degeneration of brain dopaminergic systems, a process for which there is presently no prevention. In combination with currently used drugs, cannabinoids might represent, qualitatively, a new approach to the treatment of PD, making it more effective.

http://link.springer.com/article/10.2165/00002512-200016060-00001

 

 

 

 

 

 

• Most hyperkinetic and hypokinetic movement disorders are caused by a dysfunction of basal ganglia-thalamo-cortical loops. It has been suggested that an endogenous cannabinoid tone participates in the control of movements and, therefore, the central cannabinoid system might play a role in the pathophysiology of these diseases. During the last years in humans a limited number of clinical trials demonstrated that cannabinoids might be useful in the treatment of movement disorders. Despite the lack of controlled studies there is evidence that cannabinoids are of therapeutic value in the treatment of tics in Tourette syndrome, the reduction of levodopa-induced dyskinesia in Parkinson''s disease and some forms of tremor and dystonia. It can be speculated that cannabinoid antagonists might be useful in the treatment of chorea in Huntington''s disease and hypokinetic parkinsonian syndromes.

http://www.karger.com/Article/Abstract/57153

 

• In a head to head trial of the abilities of various antioxidants to prevent glutamate toxicity, cannabidiol was superior to both a-tocopherol and ascorbate in protective capacity.

http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2000.tb06193.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

• Neuroprotective effects have been described for many cannabinoids in several neurotoxicity models.

http://onlinelibrary.wiley.com/doi/10.1046/j.0022-3042.2001.00716.x/full

 

• Lately, the ECS is emerging as a natural system of neuroprotection. Such effects have been demonstrated in adult and newborn animal models of acute and chronic neurodegenerative conditions, and postulate cannabinoids as valuable neuroprotective agents.

http://www.ingentaconnect.com/content/ben/prn/2007/00000002/00000002/art00005

 

• Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants

http://www.pnas.org/content/95/14/8268.short

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  • 2 weeks later...

Cannabis Smoking for Treatment of Parkinson's Disease

http://www.neurology.org/cgi/content/meeting_abstract/78/1_MeetingAbstracts/PD4.005

 

CBD double blind clinical trial in Parkinson’s

http://jop.sagepub.com/content/28/11/1088.full.pdf+html

 

Cannabidiol can improve complex sleep-related behaviours associated with rapid eye movement sleep behaviour disorder in Parkinson's disease patients: a case series

http://onlinelibrary.wiley.com/doi/10.1111/jcpt.12179/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

The type 1 cannabinoid receptor (CB1) is a crucial modulator of synaptic transmission in brain and has been proposed as a potential therapeutic target in Parkinson’s disease (PD), especially for treatment of levodopa-induced dyskinesias (LID). Our aim was to measure CB1

levels in brains of PD patients in vivo and to investigate the relation between CB1 availability and LID.

https://lirias.kuleuven.be/bitstream/123456789/305481/2/Van+Laere+Neurobiol+Aging.+2012+.pdf

 

Orally administered cannabis extract resulted in no objective or subjective improvement

in dyskinesias or parkinsonism.

http://www.physiol.ox.ac.uk/~xl/Carroll2004_neurol.pdf

 

In a randomized, double-blind, placebo-controlled, crossover trial (n = 7), the authors demonstrate that the cannabinoid receptor agonist nabilone significantly reduces levodopa-induced dyskinesia in PD.

http://www.neurology.org/content/57/11/2108.short

 

L-DOPA-treatment in primates disrupts the expression of A2A adenosine-CB1 cannabinoid-D2 dopamine receptor heteromers in the caudate nucleus.

http://www.researchgate.net/publication/258526041_L-DOPA-treatment_in_primates_disrupts_the_expression_of_A2A_adenosine-CB1_cannabinoid-D2_dopamine_receptor_heteromers_in_the_caudate_nucleus

 

The influence of cannabinoids on generic traits of neurodegeneration

http://onlinelibrary.wiley.com/doi/10.1111/bph.12492/full

 

Promising cannabinoid-based therapies for Parkinson’s disease: motor symptoms to neuroprotection

http://link.springer.com/article/10.1186/s13024-015-0012-0

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  • 1 year later...

i wonder if we should submit two or more at the same time.

 

one petition for all end stage conditions such as parkinsons, dementia, quadruple paralyzation , etc

 

and then a petition for each of those conditions seperately.

 

this way the panel can pick and choose or go for broke, right? or no?

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  • 3 months later...

There's over 100 preclinical studies that relate to the ECS and PD. Cannabinoids have been demonstrated to benefit the disease itself, motor and non-motor symptoms, and symptoms associated with current treatments (L-DOPA). Perhaps more importantly we have a number of double blind clinical trials, open label studies, and patient questionnaires that demonstrate the benefits of smoked and orally consumed cannabinoids in PD treatments. There are a number of clinical trials that are cited as marked failures of cannabinoids to prove efficacy in clinical settings, but the parameters of these studies cast serious doubt on any conclusions about efficacy drawn from them.

 

We have the science, but ultimately this isn't about the science. It's about the patients. What we desperately need is for PD patients from MI who derive benefit from cannabis to share their stories so we can put faces to this science.

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Women with PD walks in to Dr office and tells her Dr that she gets relief from tremors when she smokes pot. Dr says okay, I'll give you a different drug each day for four days and we'll see which works best. Here's a joint of some stale schwag with 2-9% cannabinoids. She smokes it. He watches her. Nothing happens. Cannabis is forever cited as failing to prove efficacy in scientific clinical trial.

 

Sound far fetched?

 

The first clinical trial involving smoked cannabis and PD dates back as far as 1990, and it sought to observe the impact of smoked cannabis on serious tremors of five treatment resistant patients. According to the researchers the trial came about from reports from a PD patient that described a reduction in tremors for up to three hours after smoking cannabis. While the researchers didn’t observe a significant reduction in tremors during the trial, it should be pointed out that the cannabis described in the study “approximately 1g shredded leaf” only contained 2-9% THC by weight. First, this is a huge variance. Second, at any given rate provided (2-9%) the cannabis used was extremely low quality by today’s standards and this results in less cannabinoids being delivered systemically via inhalation. While this, as well as the very parameters of the trial itself (which was highly flawed and included the use of other drugs like diazepam) cast doubt on any conclusions drawn from the trial, one fact remains: PD patients smoked marijuana cigarettes in a clinical setting and no serious adverse effects were documented, though mild drowsiness and euphoria was reported. The researchers almost reluctantly point out the possibility of smoked cannabis alleviating anxiety induced tremors, otherwise they (and others) cite this trial as a marked failure of cannabis to prove efficacy in the clinical setting for PD. Any conclusions drawn in regards to efficacy from this study should be taken with a grain of salt. (Frankel 1990)

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC488064/?page=1

 

Seem legit? There's more where that came from.

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Here's some refernces from http://www.parkinson.org/find-help/blogs/whats-hot/august-2014

 

Selected References for Medical Marijuana and Parkinson’s Disease

Chagas MH, Eckeli AL, Zuardi AW, Pena-Pereira MA, Sobreira-Neto MA, Sobreira ET, Camilo MR, Bergamaschi MM, Schenck CH, Hallak JE, Tumas V, Crippa JA. Cannabidiol can improve complex sleep-related behaviours associated with rapid eye movement sleep behaviour disorder in Parkinson's disease patients: a case series. J Clin Pharm Ther. 2014 May 21. doi: 10.1111/jcpt.12179. [Epub ahead of print] PubMed PMID: 24845114.

 

Koppel BS, Brust JC, Fife T, Bronstein J, Youssof S, Gronseth G, Gloss D. Systematic review: efficacy and safety of medical marijuana in selected neurologic disorders: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2014 Apr 29;82(17):1556-63. doi: 10.1212/WNL.0000000000000363. Review. PubMed PMID: 24778283; PubMed Central PMCID: PMC4011465.

 

Lotan I, Treves TA, Roditi Y, Djaldetti R. Cannabis (medical marijuana) treatment for motor and non-motor symptoms of Parkinson disease: an open-label observational study. Clin Neuropharmacol. 2014 Mar-Apr;37(2):41-4. doi: 10.1097/WNF.0000000000000016. PubMed PMID: 24614667.

 

Gowran A, Noonan J, Campbell VA. The multiplicity of action of cannabinoids: implications for treating neurodegeneration. CNS Neurosci Ther. 2011 Dec;17(6):637-44. doi: 10.1111/j.1755-5949.2010.00195.x. Epub 2010 Sep 28. Review. PubMed PMID: 20875047.

 

Iuvone T, Esposito G, De Filippis D, Scuderi C, Steardo L. Cannabidiol: a promising drug for neurodegenerative disorders? CNS Neurosci Ther. 2009 Winter;15(1):65-75. doi: 10.1111/j.1755-5949.2008.00065.x. Review. PubMed PMID: 19228180.

McSherry JW. Cannabis for dyskinesia in Parkinson disease: a randomized double-blind crossover study. Neurology. 2005 Mar 22;64(6):1100; author reply 1100. PubMed PMID: 15781848.

 

Carroll CB, Bain PG, Teare L, Liu X, Joint C, Wroath C, Parkin SG, Fox P, Wright D, Hobart J, Zajicek JP. Cannabis for dyskinesia in Parkinson disease: a randomized double-blind crossover study. Neurology. 2004 Oct 12;63(7):1245-50. PubMed PMID: 15477546.

 

Venderová K, Růzicka E, Vorísek V, Visnovský P. Survey on cannabis use in Parkinson's disease: subjective improvement of motor symptoms. Mov Disord. 2004 Sep;19(9):1102-6. PubMed PMID: 15372606.

 

Volkow ND, Baler RD, Compton WM, Weiss SR. Adverse health effects of marijuana use. N Engl J Med. 2014 Jun 5;370(23):2219-27. doi: 10.1056/NEJMra1402309. Review. PubMed PMID: 24897085.

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  • 4 weeks later...

Cannabis Smoking for Treatment of Parkinson's Disease

http://www.neurology.org/cgi/content/meeting_abstract/78/1_MeetingAbstracts/PD4.005

 

CBD double blind clinical trial in Parkinson’s

http://jop.sagepub.com/content/28/11/1088.full.pdf+html

 

Cannabidiol can improve complex sleep-related behaviours associated with rapid eye movement sleep behaviour disorder in Parkinson's disease patients: a case series

http://onlinelibrary.wiley.com/doi/10.1111/jcpt.12179/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

 

The type 1 cannabinoid receptor (CB1) is a crucial modulator of synaptic transmission in brain and has been proposed as a potential therapeutic target in Parkinson’s disease (PD), especially for treatment of levodopa-induced dyskinesias (LID). Our aim was to measure CB1

levels in brains of PD patients in vivo and to investigate the relation between CB1 availability and LID.

https://lirias.kuleuven.be/bitstream/123456789/305481/2/Van+Laere+Neurobiol+Aging.+2012+.pdf

 

Orally administered cannabis extract resulted in no objective or subjective improvement

in dyskinesias or parkinsonism.

http://www.physiol.ox.ac.uk/~xl/Carroll2004_neurol.pdf

 

In a randomized, double-blind, placebo-controlled, crossover trial (n = 7), the authors demonstrate that the cannabinoid receptor agonist nabilone significantly reduces levodopa-induced dyskinesia in PD.

http://www.neurology.org/content/57/11/2108.short

 

L-DOPA-treatment in primates disrupts the expression of A2A adenosine-CB1 cannabinoid-D2 dopamine receptor heteromers in the caudate nucleus.

http://www.researchgate.net/publication/258526041_L-DOPA-treatment_in_primates_disrupts_the_expression_of_A2A_adenosine-CB1_cannabinoid-D2_dopamine_receptor_heteromers_in_the_caudate_nucleus

 

The influence of cannabinoids on generic traits of neurodegeneration

http://onlinelibrary.wiley.com/doi/10.1111/bph.12492/full

 

Promising cannabinoid-based therapies for Parkinson’s disease: motor symptoms to neuroprotection

http://link.springer.com/article/10.1186/s13024-015-0012-0

got em except the first link with the smoking marijuana for parkinsons meeting

Cannabidiol can improve complex sleep in parkinsons patients.pdf

Cannabis (Medical Marijuana) Treatment for Motor and Non–Motor Symptoms of Parkinson Disease.pdf

Cannabis for dyskinesia in parkinsons disease.pdf

Effects of cannabidiol in the treatment of patients with Parkinson's disease.pdf

Efficacy and safety of medical marijuana in certain Neurologic Disorders 2014.pdf

Regional changes in type 1 cannabinoid receptor availability in parkinsons.pdf

The influence of cannabinoids on generic traits of neurodegeneration.pdf

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Anyone can submit it. It's easy to do. Been there and done that. It's the patients that testify for it that make all the difference.

right, the idiot panel wants the person submitting it to also be the one suffering from it and answer questions about it.

 

even though none of that is required by law or rule.

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right, the idiot panel wants the person submitting it to also be the one suffering from it and answer questions about it.

 

even though none of that is required by law or rule.

It was meant to be anonymous if need be. For obvious reasons in the case of medical marijuana. But there just happens to be live cameras right in your face published almost immediately. And those videos can be used for file footage forever. It's just such a farce. The process should have been private all along. These are patients not circus performers. How did we get to this extent of craziness?

We wanted new conditions really bad but to be lead down this path to get there? Is this a satire? It doesn't seem real.

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  • 1 month later...

Could we make some kind of sign for the booth?  Maybe something simple like "Do you or someone you know suffer from Parkinson's?"

Not sure what else might draw people in.  I think I have some poster board, I could whip up a nice sign.  Maybe a sign up sheet so we

could contact those interested?

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I will make up a sign stating what ever the MMMA.org approves of.

 

I think a sign would be helpful because anyone who is interested is there in front of us

and we can give and get information to move forward.

 

There is so much to do and see there that imho, an announcement might be forgotten

even for those with the best intentions to help.

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Do we have to list the potential side effects?

 

I think these are good ideas. It's something anyway. There's a fb page but I haven't posted much of anything nor have I done much cheer leading for it online. If someone is interested in taking the reigns on the page I'd be happy to turn it over. Also, a rough draft of a paper was slapped together, but I haven't looked at it since. I wouldn't be entirely opposed to posting it online so that the forum can collectively work on it. That way the focus can be more on MMMA and the cause than about anything else. Not sure how to work that logistically, or if there'd be any interest, but it's on the table. 

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