Marijuana's cannabinoids protect the brain from Alzheimer's disease

Here is more evidence that THC and CBD, cannabinoids from marijuana, can effectively protect us from the damage that leads to the development of Alzheimer's disease as well as other neurological ailments. The cannabinoid THC stimulates both the CB1 and CB2 receptors, but the cannabinoid CBD steers THC away from the CB1 receptor and over to the CB2 receptors, thus possibly activating the neuroprotective effects described in this study. With the trillion dollar threat that Alzheimer's disease poses to our national health care budget, isn't it critical that we recruit more adults to use some form of marijuana? Tell you friends and family that the most effective thing they can do to protect themselves from Alzheimer's disease is to start using cannabis--either smoking or vaporizing a small amount a few times a week, or taking some drops of a cannabis tincture before bedtime or eating a low-dose edible. What we want to do is increase the regular consumption of cannabinoids in our society because the evidence is in: using some form of marijuana regularly lowers our risks for developing numerous, serious illnesses. J Alzheimers Dis. 2013 Jan 1;354:847-58. doi: 10.3233/JAD-130137.CB2 Cannabinoid Receptor Agonist Ameliorates Alzheimer-Like Phenotype in AβPP/PS1 Mice.Aso E, Juvés S, Maldonado R, Ferrer I.SourceInstitut de Neuropatologia, Servei d'Anatomia Patològica, Abstract: The specific CB2 cannabinoid receptor agonist JWH-133 induced cognitive improvement in double AβPP/PS1 transgenic mice, a genetic model of Alzheimer's disease. This effect was more pronounced when administered at the pre-symptomatic rather than the early symptomatic stage. The cognitive improvement was associated with decreased microglial reactivity and reduced expression of pro-inflammatory cytokines IL-1β, IL-6, TNFα, and IFNγ. In addition, JWH-133 reduced the expression of active p38 and SAPK/JNK, increased the expression of inactive GSK3β, and lowered tau hyperphosphorylation at Thr181 in the vicinity of amyloid-β plaques. Moreover, JWH-133 produced a decrease in the expression of hydroxynonenal adducts, and enhanced the expression of SOD1 and SOD2 around plaques. In contrast, the chronic treatment with JWH-133 failed to modify the amyloid-β production or deposition in cortex and hippocampus. In conclusion, the present study lends support to the idea that stimulation of CB2 receptors ameliorates several altered parameters in Alzheimer's disease such as impaired memory and learning, neuroinflammation, oxidative stress damage and oxidative stress responses, selected tau kinases, and tau hyperphosphorylation around plaques.

via CB2 Cannabinoid Receptor Agonist Ameliorate... [J Alzheimers Dis. 2013] - PubMed - NCBI.

Cannabidiol from marijuana reduces cigarette consumption

As misguided politicians move to eradicate medical marijuana dispensaries, we are learning more and more about the benefits of the nonpsychoactive cannabinoid, CBD, which dealers don't sell but dispensaries do. Fight the ignorance and fight the repression! Educate the public and promote marijuana as a health-building supplement.

Addict Behav. 2013 Sep; .Cannabidiol reduces cigarette consumption in tobacco smokers: Preliminary findings. Morgan CJ, Das RK, Joye A, Curran HV, Kamboj SK.SourceClinical Psychopharmacology Unit, University College London, London, UK. .Abstract: The role of the endocannabinoid system in nicotine addiction is being increasingly acknowledged. We conducted a pilot, randomised double blind placebo controlled study set out to assess the impact of the ad-hoc use of cannabidiol CBD in smokers who wished to stop smoking. 24 smokers were randomised to receive an inhaler of CBD n=12 or placebo n=12 for one week, they were instructed to use the inhaler when they felt the urge to smoke. Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked. In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by ~40% during treatment. Results also indicated some maintenance of this effect at follow-up. These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

via Cannabidiol reduces cigarette consumption in to... [Addict Behav. 2013] - PubMed - NCBI.

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Cannabidiol from marijuana reduces cigarette consumption

As misguided politicians move to eradicate medical marijuana dispensaries, we are learning more and more about the benefits of the nonpsychoactive cannabinoid, CBD, which dealers don't sell but dispensaries do. Fight the ignorance and fight the repression! Educate the public and promote marijuana as a health-building supplement. Addict Behav. 2013 Sep; .Cannabidiol reduces cigarette consumption in tobacco smokers: Preliminary findings. Morgan CJ, Das RK, Joye A, Curran HV, Kamboj SK.SourceClinical Psychopharmacology Unit, University College London, London, UK. .Abstract: The role of the endocannabinoid system in nicotine addiction is being increasingly acknowledged. We conducted a pilot, randomised double blind placebo controlled study set out to assess the impact of the ad-hoc use of cannabidiol CBD in smokers who wished to stop smoking. 24 smokers were randomised to receive an inhaler of CBD n=12 or placebo n=12 for one week, they were instructed to use the inhaler when they felt the urge to smoke. Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked. In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by ~40% during treatment. Results also indicated some maintenance of this effect at follow-up. These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

via Cannabidiol reduces cigarette consumption in to... [Addict Behav. 2013] - PubMed - NCBI.

CBD from marijuana protects the brain from Alzheimer's disease and triggers the production of new brain cells

Like THC, the cannabinoid CBD from marijuana protects the brain from the damage that leads to Alzheimer's disease and other forms of dementia. CBD, which lacks the psychoactive effects of THC, is only available from cannabis products sold by dispensaries, dealers do not sell marijuana that doesn't get you high. Why are communities shortsightedly moving to close dispensaries? Reefer madness residue and marijuanaphobia. Speak out for medical marijuana! Cannabidiol reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis through PPARγ involvement.       Esposito G, Scuderi C, Valenza M, Togna GI, Latina V, De Filippis D, Cipriano M, Carratù MR, Iuvone T, Steardo L.SourceDepartment of Physiology and Pharmacology Vittorio Erspamer, Sapienza University of Rome, Rome, Italy.                                                                               Abstract: Peroxisome proliferator-activated receptor-γ PPARγ has been reported to be involved in the etiology of pathological features of Alzheimer's disease AD. Cannabidiol CBD, a Cannabis derivative devoid of psychomimetic effects, has attracted much attention because of its promising neuroprotective properties in rat AD models, even though the mechanism responsible for such actions remains unknown. This study was aimed at exploring whether CBD effects could be subordinate to its activity at PPARγ, which has been recently indicated as its putative binding site. CBD actions on β-amyloid-induced neurotoxicity in rat AD models, either in presence or absence of PPAR antagonists were investigated. Results showed that the blockade of PPARγ was able to significantly blunt CBD effects on reactive gliosis and subsequently on neuronal damage. Moreover, due to its interaction at PPARγ, CBD was observed to stimulate hippocampal neurogenesis. All these findings report the inescapable role of this receptor in mediating CBD actions, here reported.

via Cannabidiol reduces Aβ-induced neuroinflammation an... [PLoS One. 2011] - PubMed - NCBI.

CBD protects pig brains--new hope for politicians

CBD protects pig brains in a model of stroke. Cannabinoids, such as THC and CBD, protect the brain. Neuropharmacology. 2013 Aug;71C:282-291. doi: 10.1016/j.neuropharm.2013.03.027. Epub 2013 Apr 12.Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs: Role of 5HT1A and CB2 receptors.Pazos MR, Mohammed N, Lafuente H, Santos M, Martínez-Pinilla E, Moreno E, Valdizan E, Romero J, Pazos A, Franco R, Hillard CJ, Alvarez FJ, Martínez-Orgado J.SourceExperimental Unit, Pediatric Department, University Hospital Puerta de Hierro Majadahonda, 28222 Madrid, Spain.AbstractThe mechanisms underlying the neuroprotective effects of cannabidiol CBD were studied in vivo using a hypoxic-ischemic HI brain injury model in newborn pigs. One- to two-day-old piglets were exposed to HI for 30 min by interrupting carotid blood flow and reducing the fraction of inspired oxygen to 10%. Thirty minutes after HI, the piglets were treated with vehicle HV or 1 mg/kg CBD, alone HC or in combination with 1 mg/kg of a CB2 receptor antagonist AM630 or a serotonin 5HT1A receptor antagonist WAY100635. HI decreased the number of viable neurons and affected the amplitude-integrated EEG background activity as well as different prognostic proton-magnetic-resonance-spectroscopy H±-MRS-detectable biomarkers lactate/N-acetylaspartate and N-acetylaspartate/choline ratios. HI brain damage was also associated with increases in excitotoxicity increased glutamate/N-acetylaspartate ratio, oxidative stress decreased glutathione/creatine ratio and increased protein carbonylation and inflammation increased brain IL-1 levels. CBD administration after HI prevented all these alterations, although this CBD-mediated neuroprotection was reversed by co-administration of either WAY100635 or AM630, suggesting the involvement of CB2 and 5HT1A receptors. The involvement of CB2 receptors was not dependent on a CBD-mediated increase in endocannabinoids. Finally, bioluminescence resonance energy transfer studies indicated that CB2 and 5HT1A receptors may form heteromers in living HEK-293T cells. In conclusion, our findings demonstrate that CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A receptors are implicated in these effects.

via Mechanisms of cannabidiol neuroprotection ... [Neuropharmacology. 2013] - PubMed - NCBI.

Natural Cannabinoids Improve Dopamine Neuro... [J Alzheimers Dis. 2013] - PubMed - NCBI

Cannabis protects us from Alzheimer's and other forms of dementia and natural cannabis from a dispensary is far less expensive than Sativex and keeps money in the community and away from big pharma and foreign profiteers. There is a role for Sativex as a prescribed drug, possibly compounded with other treatments, but not as a monopoly. Natural Cannabinoids Improve Dopamine Neurotransmission and Tau and Amyloid Pathology in a Mouse Model of Tauopathy.Casarejos MJ, Perucho J, Gomez A, Muñoz MP, Fernandez-Estevez M, Sagredo O, Fernandez Ruiz J, Guzman M, de Yebenes JG, Mena MA.SourceDepartments of Neurobiology, Ramon y Cajal University Hospital, Madrid, Spain CIBERNED, Spain.AbstractCannabinoids are neuroprotective in models of neurodegenerative dementias. Their effects are mostly mediated through CB1 and CB2 receptor-dependent modulation of excitotoxicity, inflammation, oxidative stress, and other processes. We tested the effects of Sativex®, a mixture of Δ9-tetrahydrocannabinol and cannabidiol, acting on both CB1 and CB2 receptors, in parkin-null, human tau overexpressing PK-/-/TauVLW mice, a model of complex frontotemporal dementia, parkinsonism, and lower motor neuron disease. The animals received Sativex®, 4.63 mg/kg, ip, daily, for one month, at six months of age, at the onset of the clinical symptoms. We evaluated the effects of Sativex® on behavior, dopamine neurotransmission, glial activation, redox state, mitochondrial activity, and deposition of abnormal proteins. PK-/-/TauVLW mice developed the neurological deficits, but those treated with Sativex® showed less abnormal behaviors related to stress, less auto and hetero-aggression, and less stereotypy. Sativex® significantly reduced the intraneuronal, MAO-related free radicals produced during dopamine metabolism in the limbic system. Sativex® also decreased gliosis in cortex and hippocampus, increased the ratio reduced/oxidized glutathione in the limbic system, reduced the levels of iNOS, and increased those of complex IV in the cerebral cortex. With regard to tau and amyloid pathology, Sativex® reduced the deposition of both in the hippocampus and cerebral cortex of PK-/-/TauVLW mice and increased autophagy. Sativex®, even after a short administration in animals with present behavioral and pathological abnormalities, improves the phenotype, the oxidative stress, and the deposition of proteins in PK-/-/TauVLW mice, a model of complex neurodegenerative disorders.

via Natural Cannabinoids Improve Dopamine Neuro... [J Alzheimers Dis. 2013] - PubMed - NCBI.

Study Says Cannabis May Help Reverse Dementia From Alzheimer’s

Study Says Cannabis May Help Reverse Dementia From Alzheimer’s  February 14, 2013 Toke up for the sake of your brain?                                                  The Sydney Morning Herald reports: A team from Neuroscience Research Australia is in the early stages of research examining if one of the main active ingredients in cannabis, called cannabidiol, could reverse some of the symptoms of memory loss in animals. Tim Karl, a senior research fellow with the group, said cannabidiol has been found to have anti-inflammatory, antioxidant and other effects that could be beneficial for the brain. His study involved injecting cannabidiol into mice that had symptoms similiar to those seen in Alzheimer’s, as well as examining what would happen to brain cells treated with the drug. Dr Karl found that when the mice were given the cannabidiol they showed drastic improvement on parts of the tests that were related to recognising and remembering objects and other mice: “You could say it cured them.”

via Study Says Cannabis May Help Reverse Dementia From Alzheimer’s | Disinformation.

Cannabinoids: a new hope for breast cancer ... [Cancer Treat Rev. 2012] - PubMed - NCBI

Marijuana fights beast cancer, why wait for "officials" to approve it? Use it now! Family history of breast cancer? Use it now! History of poor diet and alcohol consumption? Use it now! Cancer Treat Rev. 2012 Nov;10. 2012

Cannabinoids: a new hope for breast cancer therapy?               Caffarel MM, et al., Dept. Biochemistry and Molecular Biology I, School of Biology, Complutense University-CIBERNED-IRYCIS, Madrid, Spain.                                                                                          Abstract: Breast cancer is a very common disease that affects approximately 1 in 10 women at some point in their lives. Importantly, breast cancer cannot be considered a single disease as it is characterized by distinct pathological and molecular subtypes that are treated with different therapies and have diverse clinical outcomes. Although some highly successful treatments have been developed, certain breast tumors are resistant to conventional therapies and a considerable number of them relapse. Therefore, new strategies are urgently needed, and the challenge for the future will most likely be the development of individualized therapies that specifically target each patient's tumor. Experimental evidence accumulated during the last decade supports that cannabinoids, the active components of Cannabis sativa and their derivatives, possess anticancer activity. Thus, these compounds exert anti-proliferative, pro-apoptotic, anti-migratory and anti-invasive actions in a wide spectrum of cancer cells in culture. Moreover, tumor growth, angiogenesis and metastasis are hampered by cannabinoids in xenograft-based and genetically-engineered mouse models of cancer. This review summarizes our current knowledge on the anti-tumor potential of cannabinoids in breast cancer, which suggests that cannabinoid-based medicines may be useful for the treatment of most breast tumor subtypes.Copyright © 2012 Elsevier Ltd. All rights reserved.

via Cannabinoids: a new hope for breast cancer ... [Cancer Treat Rev. 2012] - PubMed - NCBI.

US Investigators Praise Cannabinoids As Chemo Treatment

US Investigators Praise Cannabinoids As Chemo Treatment“ Cannabinoids inhibit cancer cell proliferation and should be clinically tested as chemotherapeutic agents, according to a review published in the January issue of the journal Cancer Research.Investigators at the University of Wisconsin School of Medicine and Public Health reported that the administration of cannabinoids halts the spread of a wide range of cancers, including brain cancer, prostate cancer, breast cancer, lung cancer, skin cancer, pancreatic cancer, and lymphoma. Researchers suggested that cannabinoids may offer significant advantages over standard chemotherapy treatments because the compounds are both non-toxic and can uniquely target malignant cells while ignoring healthy ones.“Cannabinoids … offer potential applications as anti-tumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival,” authors concluded. “[T]here is overwhelming evidence to suggest that cannabinoids can be explored as chemotherapeutic agents for the treatment of cancer.”"Read more: http://norml.org/news/2008/01/31/us-investigators-praise-cannabinoids-as-chemo-treatment

via US Investigators Praise Cannabinoids As Chemo Treatment | www.thctotalhealthcare.com.

Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI

CBD a plant cannabinoid found in marijuana/cannabis is a possible, effective treatment for Kaposi sarcoma. It's been about 16 years since effective anti-viral medicines were released for AIDS patients so many of you have never seen someone covered in and disfigured by purple KS lesions but anything that offers relief should be made available, not kept on Schedule one of the Controlled Substances Act. KS is not a disease that is exclusive to AIDS patients therefore CBD might benefit those who cannot use anti-retroviral drugs. Legalize the plant for goodness sake! Genes Cancer. 2012 Jul;37-8:512-20.

.Cannabidiol inhibits growth and induces programmed cell death in kaposi sarcoma-associated herpesvirus-infected endothelium.   Maor Y, Yu J, Kuzontkoski PM, Dezube BJ, Zhang X, Groopman JE.  SourceDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Abstract: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus KSHV. It is prevalent among the elderly in the Mediterranean, inhabitants of sub-Saharan Africa, and immunocompromised individuals such as organ transplant recipients and AIDS patients. Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host. When the host's immune system weakens, KSHV begins to replicate again, and active tumor growth ensues. New therapeutic approaches are needed. Cannabidiol CBD, a plant-derived cannabinoid, exhibits promising antitumor effects without inducing psychoactive side effects. CBD is emerging as a novel therapeutic for various disorders, including cancer. In this study, we investigated the effects of CBD both on the infection of endothelial cells ECs by KSHV and on the growth and apoptosis of KSHV-infected ECs, an in vitro model for the transformation of normal endothelium to Kaposi sarcoma. While CBD did not affect the efficiency with which KSHV infected ECs, it reduced proliferation and induced apoptosis in those infected by the virus. CBD inhibited the expression of KSHV viral G protein-coupled receptor vGPCR, its agonist, the chemokine growth-regulated protein α GRO-α, vascular endothelial growth factor receptor 3 VEGFR-3, and the VEGFR-3 ligand, vascular endothelial growth factor C VEGF-C. This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma.

via Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI.

Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI

CBD a plant cannabinoid found in marijuana/cannabis is a possible, effective treatment for Kaposi sarcoma. It's been about 16 years since effective anti-viral medicines were released for AIDS patients so many of you have never seen someone covered in and disfigured by purple KS lesions but anything that offers relief should be made available, not kept on Schedule one of the Controlled Substances Act. KS is not a disease that is exclusive to AIDS patients therefore CBD might benefit those who cannot use anti-retroviral drugs. Legalize the plant for goodness sake! Genes Cancer. 2012 Jul;37-8:512-20.

.Cannabidiol inhibits growth and induces programmed cell death in kaposi sarcoma-associated herpesvirus-infected endothelium.   Maor Y, Yu J, Kuzontkoski PM, Dezube BJ, Zhang X, Groopman JE.  SourceDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Abstract: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus KSHV. It is prevalent among the elderly in the Mediterranean, inhabitants of sub-Saharan Africa, and immunocompromised individuals such as organ transplant recipients and AIDS patients. Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host. When the host's immune system weakens, KSHV begins to replicate again, and active tumor growth ensues. New therapeutic approaches are needed. Cannabidiol CBD, a plant-derived cannabinoid, exhibits promising antitumor effects without inducing psychoactive side effects. CBD is emerging as a novel therapeutic for various disorders, including cancer. In this study, we investigated the effects of CBD both on the infection of endothelial cells ECs by KSHV and on the growth and apoptosis of KSHV-infected ECs, an in vitro model for the transformation of normal endothelium to Kaposi sarcoma. While CBD did not affect the efficiency with which KSHV infected ECs, it reduced proliferation and induced apoptosis in those infected by the virus. CBD inhibited the expression of KSHV viral G protein-coupled receptor vGPCR, its agonist, the chemokine growth-regulated protein α GRO-α, vascular endothelial growth factor receptor 3 VEGFR-3, and the VEGFR-3 ligand, vascular endothelial growth factor C VEGF-C. This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma.

via Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI.

Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience

Why do they bother to develop and test these drugs when it is well-established that the phytocannabinoids generated by the cannabis plant--especially THC and CBD--have unique and unequaled anti-Alzheimer's activities? It is quite clear that these cannabinoids work on several levels to protect the brain from changes that lead to various forms of dementia. THC and CBD work against inflammation and oxidation while neutralizing toxic compounds such as TNF--tumor necrosis factor and cannabinoids dissolve the beta-amyloid plaque while reducing the production of tau scar tissue and triggering the production of healthy replacement neurons. Big pharma just needs to acknowledge that nature does it better. Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience

Alzheimer’s disease is a debilitating neurodegenerative disease characterized by dementia and memory loss. It is the sixth leading cause of death in the United States, where more than 5 million people are affected. There is clearly a need for more effective therapies that address this and other neurodegenerative diseases; however, the research and development (R&D) efforts put forth by pharmaceutical companies have rarely been successful, as illustrated by the recent failure of the Alzheimer’s drug bapineuzumab in clinical trials.

Johnson & Johnson and Pfizer in separate press releases on August 6, 2012, announced the discontinuation of their joint Phase III clinical development of intravenous (IV) bapineuzumab in mild-to-moderate cases of Alzheimer’s disease. This comes on the heels of disappointing results from the clinical trial Study 301, in which bapineuzumab was being tested in patients who are non-carriers of the ApoE4 (Apolipoprotein E epsilon 4) gene. Results indicated that bapineuzumab did not satisfy either cognitive or functional performance endpoints. These disappointing study results follow similar results announced on July 23 from Study 302, in which bapineuzumab also failed to meet clinical endpoints in ApoE4 carrier patients.

Bapineuzumab IV is an antibody that targets the beta-amyloid protein (A), which is believed to cause brain toxicity and is implicated in the pathology of Alzheimer’s disease.

via Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience.

Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience

Why do they bother to develop and test these drugs when it is well-established that the phytocannabinoids generated by the cannabis plant--especially THC and CBD--have unique and unequaled anti-Alzheimer's activities? It is quite clear that these cannabinoids work on several levels to protect the brain from changes that lead to various forms of dementia. THC and CBD work against inflammation and oxidation while neutralizing toxic compounds such as TNF--tumor necrosis factor and cannabinoids dissolve the beta-amyloid plaque while reducing the production of tau scar tissue and triggering the production of healthy replacement neurons. Big pharma just needs to acknowledge that nature does it better. Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience

Alzheimer’s disease is a debilitating neurodegenerative disease characterized by dementia and memory loss. It is the sixth leading cause of death in the United States, where more than 5 million people are affected. There is clearly a need for more effective therapies that address this and other neurodegenerative diseases; however, the research and development (R&D) efforts put forth by pharmaceutical companies have rarely been successful, as illustrated by the recent failure of the Alzheimer’s drug bapineuzumab in clinical trials.

Johnson & Johnson and Pfizer in separate press releases on August 6, 2012, announced the discontinuation of their joint Phase III clinical development of intravenous (IV) bapineuzumab in mild-to-moderate cases of Alzheimer’s disease. This comes on the heels of disappointing results from the clinical trial Study 301, in which bapineuzumab was being tested in patients who are non-carriers of the ApoE4 (Apolipoprotein E epsilon 4) gene. Results indicated that bapineuzumab did not satisfy either cognitive or functional performance endpoints. These disappointing study results follow similar results announced on July 23 from Study 302, in which bapineuzumab also failed to meet clinical endpoints in ApoE4 carrier patients.

Bapineuzumab IV is an antibody that targets the beta-amyloid protein (A), which is believed to cause brain toxicity and is implicated in the pathology of Alzheimer’s disease.

via Alzheimer’s Drug Failure: Implications for Future R&D in Neuroscience.

Chemopreventive effect of the non-psychotro... [J Mol Med (Berl). 2012] - PubMed - NCBI

Chemoprevention of disease with cannabis--this is what everyone should be talking about. Using marijuana can protect you from serious illnesses by reducing inflammation, counteracting harmful oxidation, down regulating the production of harmful chemicals in the body, stimulating the production of beneficial chemicals in the body and triggering our intrinsic repair mechanisms, this is big news! We need to encourage everyone we meet to consider embracing cannabis supplementation to guard themselves from Alzheimer's disease, cancer, diabetes and more with chemoprevention.  

J Mol Med (Berl). 2012 Aug;90(8):925-34. Epub 2012 Jan 10.

Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer.

Aviello G, Romano B, Borrelli F, Capasso R, Gallo L, Piscitelli F, Di Marzo V, Izzo AA.

Source

Department of Experimental Pharmacology, Endocannabinoid Research Group, University of Naples Federico II, Naples, Italy.

Abstract

Colon cancer affects millions of individuals in Western countries. Cannabidiol, a safe and non-psychotropic ingredient of Cannabis sativa, exerts pharmacological actions (antioxidant and intestinal antinflammatory) and mechanisms (inhibition of endocannabinoid enzymatic degradation) potentially beneficial for colon carcinogenesis. Thus, we investigated its possible chemopreventive effect in the model of colon cancer induced by azoxymethane (AOM) in mice. AOM treatment was associated with aberrant crypt foci (ACF, preneoplastic lesions), polyps, and tumour formation, up-regulation of phospho-Akt, iNOS and COX-2 and down-regulation of caspase-3. Cannabidiol-reduced ACF, polyps and tumours and counteracted AOM-induced phospho-Akt and caspase-3 changes. In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARγ-antagonists sensitive manner. It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.

PMID:

22231745

[PubMed - in process]

via Chemopreventive effect of the non-psychotro... [J Mol Med (Berl). 2012] - PubMed - NCBI.

Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

The non-psychoactive cannabinoid CBD has powerful anti-tumor effects without toxic side-effects! It is only available at medical marijuana dispensaries, in certain states with protections for cannabis-using patients. Hopefully the war on dispensaries will end in Obama's 2nd term because street dealers do not sell cannabis products that don't get you high. If someone you love has breast cancer or another serious cancer, get to a medical state and get some CBD marijuana, or better yet concentrate. And raise hell to your elected officials about how prohibition harms us all! It's time to humiliate the defenders of this immoral prohibition policy as enemies of public health and human decency. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

Sean D. McAllister, et al.

Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol CBD, a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness. [Mol Cancer Ther 2007;611:2921–7]

via Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.

Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

The non-psychoactive cannabinoid CBD has powerful anti-tumor effects without toxic side-effects! It is only available at medical marijuana dispensaries, in certain states with protections for cannabis-using patients. Hopefully the war on dispensaries will end in Obama's 2nd term because street dealers do not sell cannabis products that don't get you high. If someone you love has breast cancer or another serious cancer, get to a medical state and get some CBD marijuana, or better yet concentrate. And raise hell to your elected officials about how prohibition harms us all! It's time to humiliate the defenders of this immoral prohibition policy as enemies of public health and human decency. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

Sean D. McAllister, et al.

Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol CBD, a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness. [Mol Cancer Ther 2007;611:2921–7]

via Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.

Marijuana And Cancer: Scientists Find Cannabis Compound Stops Metastasis In Aggressive Cancers

Marijuana may be your best bet for beating cancer! A pair of scientists at California Pacific Medical Center in San Francisco has found that a compound derived from marijuana could stop metastasis in many kinds of aggressive cancer, potentially altering the fatality of the disease forever."It took us about 20 years of research to figure this out, but we are very excited," said Pierre Desprez, one of the scientists behind the discovery, to The Huffington Post. "We want to get started with trials as soon as possible."The San Francisco Chronicle first reported on the finding, which has already undergone both laboratory and animal testing, and is awaiting permission for clinical trials in humans.Desprez, a molecular biologist, spent decades studying ID-1, the gene that causes cancer to spread. Meanwhile, fellow researcher Sean McAllister was studying the effects of Cannabidiol, or CBD, a non-toxic, non-psychoactive chemical compound found in the cannabis plant. Finally, the pair collaborated, combining CBD and cells containing high levels of ID-1 in a petri dish."What we found was that his Cannabidiol could essentially 'turn off' the ID-1," Desprez told HuffPost. The cells stopped spreading and returned to normal."We likely would not have found this on our own," he added. "That's why collaboration is so essential to scientific discovery."Desprez and McAllister first published a paper about the finding in 2007. Since then, their team has found that CBD works both in the lab and in animals. And now, they've found even more good news."We started by researching breast cancer," said Desprez. "But now we've found that Cannabidiol works with many kinds of aggressive cancers--brain, prostate--any kind in which these high levels of ID-1 are present."

via Marijuana And Cancer: Scientists Find Cannabis Compound Stops Metastasis In Aggressive Cancers.

Translational Psychiatry - Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia

The cannabinoid cannabidiol, (CBD)--found in marijuana--has remarkable effects against schizophrenic psychosis. It also shows great promise for treating breast cancer and diabetes. The only place you can get medications, i.e. cannabis and cannabis remedies with CBD, is from dispensaries in states with medical marijuana laws. Dispensaries contract with growers to purchase high CBD strains and the products are then tested by analytical labs to ascertain the levels of CBD and THC. The availability of these products has salvaged many, many patients' health and relieved an immense amount of suffering. Why are politicians who claim to be compassionate and concerned about citizens' health care working so hard to close down dispensaries? Terrible, terrible politicians like Dianne Feinstein remain arrogantly and smugly ignorant and cling to out-dated reefer-madness based policies with their greedy blood-stained talons not giving a damn about the misery of cancer, AIDS, Alzheimer's disease, diabetes and mental illness patients. Citation: Translational Psychiatry 2012 2, e94; doi:10.1038/tp.2012.15Published online 20 March 2012Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophreniaF M Leweke1,2, D Piomelli3,4, F Pahlisch1,3, D Muhl2,3, C W Gerth2, C Hoyer1,2, J Klosterkötter2, M Hellmich5 and D Koethe1,2 1Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany 2Department of Psychiatry and Psychotherapy, University of Cologne, Cologne, Germany 3Department of Pharmacology and Biological Chemistry, University of California, Irvine, CA, USA 4The Unit of Drug Discovery and Development, Italian Institute of Technology, Genova, Italy 5Institute for Medical Statistics, Informatics, and Epidemiology, University of Cologne, Cologne, GermanyCorrespondence: Professor FM Leweke, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, Medical Faculty Mannheim, J5, 68159 Mannheim, Germany. E-mail: leweke@cimh.de; D Piomelli, Department of Pharmacology and Biological Chemistry, University of California, Irvine, 3101 Gillespie Neuroscience Facility, Irvine, CA 91697-4625, USA. E-mail: piomelli@uci.eduReceived 13 October 2011; Revised 9 January 2012; Accepted 30 January 2012Top of pageAbstractCannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid anandamide. We previously reported that an elevation of anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms. Furthermore, enhanced anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition. In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.Keywords:anandamide; cannabidiol; endocannabinoid; fatty acid amide hydrolase; human; schizophrenia

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CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE... [Br J Pharmacol. 2012] - PubMed - NCBI

Again we see the amazing anti-tumor effects of the unique compounds produced by the marijuana/cannabis plant. Again we ask, why is growing, using or distributing this plant illegal? According to the researchers "CBD could represent a potential effective agent in cancer therapy" CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE MECHANISMS.

Solinas M, Massi P, Cantelmo A, Cattaneo M, Cammarota R, Bartolini D, Cinquina V, Valenti M, Vicentini L, Noonan D, Albini A, Parolaro D.

Source

Department of Biomedical, Computer and Communication Sciences, University of Insubria, Busto Arsizio (VA), Italy, Department of Pharmacology, Chemotherapy and Toxicology, University of Milan, 20129 Milan, Italy, Oncology Research Laboratory, Science and Technology Park, IRCCS MultiMedica, 20138 Milan, Italy, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy.

Abstract

Background and purpose: Several studies demonstrated anti-proliferative and pro-apoptotic actions of cannabinoids on several tumours, together with their anti-angiogenic properties. The non-psychoactive cannabinoid cannabidiol (CBD) effectively inhibits in vitro and in vivo the growth of different types of tumours and down-regulates some pro-angiogenic signal produced by glioma cells. As its anti-angiogenic properties have not been thoroughly investigated to date, and given its very favorable pharmacological and toxicological profile, here we evaluated CBD ability to modulate tumour angiogenesis. Experimental approach: We firstly evaluated CBD effect on human umbilical vein endothelial cell (HUVEC) proliferation and viability- through MTT assay and FACS analysis-and in vitro motility-both in a classical Boyden chamber test and in a wound-healing assay. We next investigated CBD effects on different angiogenesis-related proteins released by HUVECs, using an angiogenic Array Kit and an enzyme-linked immunosorbent assay (ELISA) directed at MMP2. Afterwards we evaluated in vitro angiogenesis in treated HUVECs invading a Matrigel layer and in HUVEC spheroids embedded into collagen gels. We further characterized CBD effects using a Matrigel sponge model of in vivo angiogenesis. Key results: CBD induced HUVEC cytostasis without inducing apoptosis, inhibited HUVEC migration, invasion, and sprouting in vitro, and angiogenesis in vivo in matrigel sponges. These effects were associated with down-modulation of several angiogenesis-related molecules. Conclusions and Implications: This study reveals that CBD inhibits angiogenesis by multiple mechanisms. Its dual effect on both tumour and endothelial cells reinforces the hypothesis that CBD could represent a potential effective agent in cancer therapy. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

via CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE... [Br J Pharmacol. 2012] - PubMed - NCBI.

CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE... [Br J Pharmacol. 2012] - PubMed - NCBI

Again we see the amazing anti-tumor effects of the unique compounds produced by the marijuana/cannabis plant. Again we ask, why is growing, using or distributing this plant illegal? According to the researchers "CBD could represent a potential effective agent in cancer therapy" CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE MECHANISMS.

Solinas M, Massi P, Cantelmo A, Cattaneo M, Cammarota R, Bartolini D, Cinquina V, Valenti M, Vicentini L, Noonan D, Albini A, Parolaro D.

Source

Department of Biomedical, Computer and Communication Sciences, University of Insubria, Busto Arsizio (VA), Italy, Department of Pharmacology, Chemotherapy and Toxicology, University of Milan, 20129 Milan, Italy, Oncology Research Laboratory, Science and Technology Park, IRCCS MultiMedica, 20138 Milan, Italy, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy.

Abstract

Background and purpose: Several studies demonstrated anti-proliferative and pro-apoptotic actions of cannabinoids on several tumours, together with their anti-angiogenic properties. The non-psychoactive cannabinoid cannabidiol (CBD) effectively inhibits in vitro and in vivo the growth of different types of tumours and down-regulates some pro-angiogenic signal produced by glioma cells. As its anti-angiogenic properties have not been thoroughly investigated to date, and given its very favorable pharmacological and toxicological profile, here we evaluated CBD ability to modulate tumour angiogenesis. Experimental approach: We firstly evaluated CBD effect on human umbilical vein endothelial cell (HUVEC) proliferation and viability- through MTT assay and FACS analysis-and in vitro motility-both in a classical Boyden chamber test and in a wound-healing assay. We next investigated CBD effects on different angiogenesis-related proteins released by HUVECs, using an angiogenic Array Kit and an enzyme-linked immunosorbent assay (ELISA) directed at MMP2. Afterwards we evaluated in vitro angiogenesis in treated HUVECs invading a Matrigel layer and in HUVEC spheroids embedded into collagen gels. We further characterized CBD effects using a Matrigel sponge model of in vivo angiogenesis. Key results: CBD induced HUVEC cytostasis without inducing apoptosis, inhibited HUVEC migration, invasion, and sprouting in vitro, and angiogenesis in vivo in matrigel sponges. These effects were associated with down-modulation of several angiogenesis-related molecules. Conclusions and Implications: This study reveals that CBD inhibits angiogenesis by multiple mechanisms. Its dual effect on both tumour and endothelial cells reinforces the hypothesis that CBD could represent a potential effective agent in cancer therapy. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

via CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE... [Br J Pharmacol. 2012] - PubMed - NCBI.