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.

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.

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.

Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI

The inflammatory compound, C-reactive protein, is involved in the development of Alzheimer's disease, other forms of dementia, heart disease, diabetes and most likely cancer and arthritis. A solid study of a large population sample found that people who smoked marijuana at least three times per week had half of the blood levels of C-reactive protein as those who did not use marijuana (Decreased prevalence of diabetes in marijuana users, 2012). This is more evidence that responsible marijuana use benefits human health by preventing disease-friendly internal environments,  interrupting disease processes. and triggering repair mechanisms. Neurochem Int. 2012 Feb                                                       Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer's disease.         Bi BT, Lin HB, Cheng YF, Zhou H, Lin T, Zhang MZ, Li TJ, Xu JP.SourceDepartment of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.                                                                         Abstract: C-reactive protein CRP and β-amyloid protein Aβ are involved in the development of Alzheimer's disease AD. However, the relationship between CRP and Aβ production is unclear. In vitro and in vivo experiments were performed to investigate the association of CRP with Aβ production. Using the rat adrenal pheochromocytoma cell line PC12 cells to mimic neurons, cytotoxicity was evaluated by cell viability and supernatant lactate dehydrogenase LDH activity. The levels of amyloid precursor protein APP, beta-site APP cleaving enzyme BACE-1, and presenilins PS-1 and PS-2 were investigated using real-time polymerase chain reaction and Western blotting analysis. Aβ1-42 was measured by enzyme-linked immunosorbent assay. The relevance of CRP and Aβ as well as potential mechanisms were studied using APP/PS1 transgenic Tg mice. Treatment with 0.5-4.0 μM CRP for 48 h decreased cell viability and increased LDH leakage in PC12 cells. Incubation with CRP at a sub-toxic concentration of 0.2 μM increased the mRNA levels of APP, BACE-1, PS-1, and PS-2, as well as Aβ1-42 production. CRP inhibitor reversed the CRP-induced upregulations of the mRNA levels of APP, BACE-1, PS-1, and PS-2, and the protein levels of APP, BACE-1, PS-1, and Aβ1-42, but did not reversed Aβ1-42 cytotoxicity. The cerebral levels of CRP and Aβ1-42 in APP/PS1 Tg mice were positively correlated, accompanied with the elevated mRNA expressions of serum amyloid P component SAP, complement component 1q C1q, and tumor necrosis factor-α TNF-α. These results suggest that CRP cytotoxicity is associated with Aβ formation and Aβ-related markers expressions; CRP and Aβ were relevant in early-stage AD; CRP may be an important trigger in AD pathogenesis.

via Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI.

Marijuana protects the brain from Alzheimer's disease better than any available drugs

News Release

Marijuana's Active Ingredient Shown to Inhibit Primary Marker of Alzheimer's Disease

Discovery Could Lead to More Effective Treatments

LA JOLLA, CA, August 9, 2006 - Scientists at The Scripps Research Institute have found that the active ingredient in marijuana, tetrahydrocannabinol or THC, inhibits the formation of amyloid plaque, the primary pathological marker for Alzheimer's disease. In fact, the study said, THC is "a considerably superior inhibitor of [amyloid plaque] aggregation" to several currently approved drugs for treating the disease.

The study was published online August 9 in the journal Molecular Pharmaceutics, a publication of the American Chemical Society.

According to the new Scripps Research study, which used both computer modeling and biochemical assays, THC inhibits the enzyme acetylcholinesterase (AChE), which acts as a "molecular chaperone" to accelerate the formation of amyloid plaque in the brains of Alzheimer victims. Although experts disagree on whether the presence of beta-amyloid plaques in those areas critical to memory and cognition is a symptom or cause, it remains a significant hallmark of the disease. With its strong inhibitory abilities, the study said, THC "may provide an improved therapeutic for Alzheimer's disease" that would treat "both the symptoms and progression" of the disease.

"While we are certainly not advocating the use of illegal drugs, these findings offer convincing evidence that THC possesses remarkable inhibitory qualities, especially when compared to AChE inhibitors currently available to patients," said Kim Janda, Ph.D., who is Ely R. Callaway, Jr. Professor of Chemistry at Scripps Research, a member of The Skaggs Institute for Chemical Biology, and director of the Worm Institute of Research and Medicine. "In a test against propidium, one of the most effective inhibitors reported to date, THC blocked AChE-induced aggregation completely, while the propidium did not. Although our study is far from final, it does show that there is a previously unrecognized molecular mechanism through which THC may directly affect the progression of Alzheimer's disease."

As the new study points out, any new treatment that could halt or even slow the progression of Alzheimer's disease would have a major impact on the quality of life for patients, as well as reducing the staggering health care costs associated with the disease.

Alzheimer's disease is the leading cause of dementia among the elderly, and the numbers are growing. The Alzheimer's Association estimates 4.5 million Americans have the disease, a figure that could reach as high as 16 million by 2050. A survey by the National Center for Health Statistics noted that half of all nursing home residents have Alzheimer's disease or a related disorder. The costs of caring for Alzheimer's patients are at least $100 billion annually, according to the National Institute on Aging.

Over the last two decades, the causes of Alzheimer's disease have been clarified through extensive biochemical and neurobiological studies, leading to an assortment of possible therapeutic strategies including interference with beta amyloid metabolism, the focus of the Scripps Research study.

The cholinergic system - the nerve cell system in the brain that uses acetylcholine (Ach) as a neurotransmitter - is the most dramatic of the neurotransmitter systems affected by Alzheimer's disease. Levels of acetylcholine, which was first identified in 1914, are abnormally low in the brains of Alzheimer's patients. Currently, there are four FDA-approved drugs that treat the symptoms of Alzheimer's disease by inhibiting the active site of acetylcholinesterase, the enzyme responsible for the degradation of acetylcholine.

"When we investigated the power of THC to inhibit the aggregation of beta-amyloid," Janda said, "we found that THC was a very effective inhibitor of acetylcholinesterase. In addition to propidium, we also found that THC was considerably more effective than two of the approved drugs for Alzheimer's disease treatment, donepezil (Aricept ®) and tacrine (Cognex ®), which reduced amyloid aggregation by only 22 percent and 7 percent, respectively, at twice the concentration used in our studies. Our results are conclusive enough to warrant further investigation."

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.

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.

The pacemaker implanted in the brain that can prevent Alzheimer's patients losing their memory | Mail Online

Using cannabis is less expensive and does not require "delicate" brain surgery as does this treatment. There is a growing body of data which proves that marijuana/cannabis use prevents environments that lead to Alzheimer's, reduces inflammation, breaks up plaque and scar tissue in the brain and triggers the production of healthy new neurons to replace the damaged ones. Euphoranoia and marijuanaphobia and reefer madness are robbing humanity of safe, effective and inexpensive preventatives and remedies for the most devastating sicknesses which plague us. Marijuana prohibition harms us all. The 'pacemaker' implanted in the brain to prevent Alzheimer's patients losing their memory, as possible means reversing cognitive decline. Early trials show the device appears to keep brain neurons active. High hopes will be viable alternative to drug treatments.

By Anna Hodgekiss 5 December 2012 | UPDATED: 06:20 EST, 10 A ‘pacemaker’ has been implanted in to the brain of an Alzheimer's patient in a bid to reduce memory loss. The device, which uses deep brain stimulation, has already been used in thousands of people with Parkinson’s disease as possible means of boosting memory and reversing cognitive decline.Now the first patient in the US has undergone the delicate surgery to try and halt the effects of dementia, which slowly robs its mostly elderly victims of a lifetime of memories and the ability to perform the simplest of daily tasks.

via The pacemaker implanted in the brain that can prevent Alzheimer's patients losing their memory | Mail Online.

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.

Ginkgo Won't Prevent Alzheimer's, Study Finds - but Yes Weed Can

Marijuana is the Most Effective Herbal Remedy Known to Mankind Marijuana remains your best bet for protecting yourself from, or even treating yourself for, Alzheimer's disease! Here is a report that one herbal remedy, Ginko biloba has no anti-Alzheimer's activity, followed by excerpts from a Scripps study that proves that THC, the psychoactive cannabinoid in marijuana, is the best-know remedy for the pathology of Alzheimer's disease. But the federal government will not fund nor permit studies on how to utilize this compound to help us because it is so involved with maintaining the war on marijuana in order to fill prison cells for the prison-industrial complex. Even if you've never thought of smoking marijuana and are totally disinterested in anything having to do with "High Times" culture, you must understand that the prohibition of cannabis/marijuana is harming you by preventing you and your loved ones from having safe access to remedies that can protect us all from terrible illnesses.

WEDNESDAY, Sept. 5 HealthDay News -- Yet another study, this one by French researchers, finds that the herbal supplement ginkgo biloba won't prevent or delay Alzheimer's disease."One would hope that this would be the final nail in the coffin for ginkgo," said Dr. Sam Gandy, the Mount Sinai chair in Alzheimer's Disease Research and associate director of the Mount Sinai Alzheimer's Disease Research Center in New York City. "Dead and buried. Enough said. Time to move on."The report is published in the Sept. 6 online edition of The Lancet Neurology.

via Ginkgo Won't Prevent Alzheimer's, Study Finds - US News and World Report.

From the Scripps Research Institute, August 9, 2006: We demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.