Marijuana Kills MRSA and Inhibits Prions That Cause Neurodegenerative Disease; Still Recognized by Feds As a Dangerous Drug

“Research indicates that marijuana could effectively fight off MRSA, as well as prions — the proteins that cause mad cow disease and Creutzfeld-Jakob disease.”

(Photo : Flickr, "it was 3 a.m.") Pot's constituent molecules kill bacteria and inhibit the formation of prions, a protein that can cause neurodegenerative diseases.

“New research reveals that several marijuana ingredients exhibit a potent antibiotic capacity in cases of methicillin-resistant Staphylococcus aureus (MRSA) infections as well as the ability to fight off proteins called prions that can lead to Mad Cow disease and Creutzfeld-Jakob disease (CDJ).”

More: http://www.medicaldaily.com/articles/17941/20130730/marijuana-mrsa-prions-mad-cow-disease.htm

Cannabis abuse is associated with better emotional memory in schizophrenia: A functional magnetic resonance imaging study.

 “…we performed a functional magnetic resonance imaging study of emotional memory in schizophrenia patients with cannabis abuse…

  These results are consistent with previous findings showing that cannabis abuse is associated with fewer negative symptoms and better cognitive functioning in schizophrenia…”

http://www.ncbi.nlm.nih.gov/pubmed/23906663

Cannabidivarin-rich cannabis extracts are anticonvulsant in mouse and rat via a CB1 receptor-independent mechanism.

“Epilepsy is the most prevalent neurological disease and is characterised by recurrent seizures. Here we investigate: (i) the anticonvulsant profiles of cannabis-derived botanical drug substances (BDS) rich in cannabidivarin (CBDV) and containing cannabidiol (CBD) in acute in vivo seizure models and (ii) the binding of CBDV BDSs and their components at cannabinoid CB1 receptors.

CDBV BDSs exerted significant anticonvulsant effects… 

CONCLUSIONS AND IMPLICATIONS:

CBDV BDSs exerted significant anticonvulsant effects in three models of seizure that were not mediated by the CB1 cannabinoid receptor, and were of comparable efficacy to purified CBDV.

These findings strongly support the further clinical development of CBDV BDSs for treatment of epilepsy.”

http://www.ncbi.nlm.nih.gov/pubmed/23902406

“Cannabidivarin is anticonvulsant in mouse and rat… These results indicate that CBDV is an effective anticonvulsant in a broad range of seizure models.”  http://www.ncbi.nlm.nih.gov/pubmed/22970845

Evaluation of the potential of the phytocannabinoids, cannabidivarin (CBDV) and Δ9 -tetrahydrocannabivarin (THCV), to produce CB1 receptor inverse agonism symptoms of nausea in rats.

“The cannabinoid 1(CB1 ) receptor inverse agonists/antagonists, rimonabant (SR141716, SR) and AM251, produce nausea and potentiate toxin-induced nausea by inverse agonism (rather than antagonism) of the CB1 receptor. Here, we evaluated two phytocannabinoids, cannabidivarin (CBDV) and Δ9 -tetrahydrocannabivarin (THCV) for their ability to produce these behavioural effects characteristic of CB1 receptor inverse agonism in rats.

…we investigated the potential of THCV and CBDV to produce conditioned gaping (measure of nausea-induced behaviour),..

THC, THCV  and CBDV suppressed LiCl-induced conditioned gaping, suggesting anti-nausea potential…

The pattern of findings indicates that neither THCV nor CBDV produced a behavioural profile characteristic of CB1 receptor inverse agonists.

As well, these compounds may have therapeutic potential in reducing nausea.”

http://www.ncbi.nlm.nih.gov/pubmed/23902479

Peripherally restricted CB1 receptor blockers.

“Antagonists (inverse agonists) of the cannabinoid-1 (CB1) receptor showed promise as new therapies for controlling obesity and related metabolic function/liver disease.

These agents, representing diverse chemical series, shared the property of brain penetration due to the initial belief that therapeutic benefit was mainly based on brain receptor interaction. However, undesirable CNS-based side effects of the only marketed agent in this class, rimonabant, led to its removal, and termination of the development of other clinical candidates soon followed. Re-evaluation of this approach has focused on neutral or peripherally restricted (PR) antagonists.

Supporting these strategies, pharmacological evidence indicates most if not all of the properties of globally acting agents may be captured by molecules with little brain presence. Methodology that can be used to eliminate BBB penetration and the means (in vitro assays, tissue distribution and receptor occupancy determinations, behavioral paradigms) to identify potential agents with little brain presence is discussed.

Focus will be on the pharmacology supporting the contention that reported agents are truly peripherally restricted. Notable examples of these types of compounds are: TM38837 (structure not disclosed); AM6545 (8); JD5037 (15b); RTI-12 (19).”

http://www.ncbi.nlm.nih.gov/pubmed/23902803

Anandamide, Cannabinoid Type 1 Receptor, and NMDA Receptor Activation Mediate Non-Hebbian Presynaptically Expressed Long-Term Depression at the First Central Synapse for Visceral Afferent Fibers.

“Presynaptic long-term depression (LTD) of synapse efficacy generally requires coordinated activity between presynaptic and postsynaptic neurons and a retrograde signal synthesized by the postsynaptic cell in an activity-dependent manner.

In this study, we examined LTD in the rat nucleus tractus solitarii (NTS), a brainstem nucleus that relays homeostatic information from the internal body to the brain.

We found that coactivation of N-methyl-D-aspartate receptors (NMDARs) and type 1 cannabinoid receptors (CB1Rs) induces LTD at the first central excitatory synapse between visceral fibers and NTS neurons. This LTD is presynaptically expressed. However, neither postsynaptic activation of NMDARs nor postsynaptic calcium influx are required for its induction. Direct activation of NMDARs triggers cannabinoid-dependent LTD.  In addition, LTD is unaffected by blocking 2-arachidonyl-glycerol synthesis, but its induction threshold is lowered by preventing fatty acid degradation.

Altogether, our data suggest that LTD in NTS neurons may be entirely expressed at the presynaptic level by local anandamide synthesis.”

http://www.ncbi.nlm.nih.gov/pubmed/23904599

Active Ingredient in Marijuana Kills Brain Cancer Cells – ABCNews

ABC News

 

 

“New research out of Spain suggests that THC — the active ingredient in marijuana — appears to prompt the death of brain cancer cells.

The finding is based on work with mice designed to carry human cancer tumors, as well as from an analysis of THC’s impact on tumor cells extracted from two patients coping with a highly aggressive form of brain cancer.

Explaining that the introduction of THC into the brain triggers a cellular self-digestion process known as “autophagy,” study co-author Guillermo Velasco said his team has isolated the specific pathway by which this process unfolds, and noted that it appears “to kill cancer cells, while it does not affect normal cells…”

 The findings were published in the April issue of The Journal of Clinical Investigation.”: http://www.jci.org/articles/view/37948

More: http://abcnews.go.com/Health/Healthday/story?id=7235037&page=1

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells” Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

THC, found in cannabis, shown to be effective in the treatment of brain tumors

“In 2000, scientists at the Complutense University of Madrid carried out an extensive experiment, testing the effects of THC on cancerous brain cells in laboratory rats. Their discoveries were nothing short of amazing, as THC had effectively managed to destroy all cancer cells, while leaving healthy cells unaffected.
 
 Research into the effects of THC on glioblastoma would have had the potential to revolutionize available cancer treatments, yet due to insufficient funding and poor public exposure, the science team was unable to further their research.Manuel Guzman explained that “cannabinoids are selective antitumor compounds, as they can kill tumor cells without affecting their non-transformed counterparts.” In contrast to this, chemotherapy, the prevalent anticancer treatment of today, consists of a combination of antineoplastic drugs that have devastating physical and psychological side-effects… 
 
THC works by triggering the build-up of a chemical messenger known as ceramide, which in turn induces apoptosis (or programmed cell death) in mutated tumor cells.
Subsequent research into the properties of THC has revealed that it is among the very few naturally occurring, harmless substances that are capable of inducing programmed cell death in cancerous cells. Other substances with this property include anandamide, other cannabinoids and tumor necrosis factors produced by the immune system in its attempt to fight cancer.
 
After months of effort to obtain funding for testing the medical effects of THC on human tissues, the Madrid science team was forced to abandon this project, although there is currently no effective treatment available for malignant brain tumors.” 
 
 

Cannabidiol potentiates pharmacological effects of Delta(9)-tetrahydrocannabinol via CB(1) receptor-dependent mechanism.

“Cannabidiol, a non-psychoactive component of cannabis, has been reported to have interactions with Delta(9)-tetrahydrocannabinol (Delta(9)-THC)…

In the present study, we investigated whether cannabidiol modulates the pharmacological effects of Delta(9)-THC…

Cannabidiol potentiated pharmacological effects of Delta(9)-THC via CB(1) receptor-dependent mechanism.

These findings may contribute in setting the basis for interaction of cannabinoids and to find a cannabinoid mechanism in central nervous system.”

http://www.ncbi.nlm.nih.gov/pubmed/18021759

Marijuana Compounds Possess Synergistic Anti-Cancer Effects, Study Says

“Marijuana’s active compounds act synergistically to inhibit the growth of cancer cells and induce malignant cell death, according to preclinical trial data published online by the journal Molecular Cancer Therapeutics.

Investigators at the University of California, Pacific Medical Center Research Institute assessed whether the administration of the non-psychoactive cannabidiol would enhance the anti-cancer effects of THC on glioblastoma (brain cancer) cells.

Researchers reported that a combination of cannabinoids showed greater anti-cancer activity than the administration of either compound individually. “We discovered that cannabidiol enhanced the ability of THC to inhibit cell proliferation and induce cell cycle arrest and apoptosis (programmed cell death),” authors reported.

Investigators concluded: “Individually, THC and cannabidiol can activate distinct pathways in glioblastoma cells that ultimately culminate in inhibition of cancer cell growth and invasion as well as induction of cell death. We hypothesized that, if the individual agents were combined, a convergence on shared pathways may ensue, leading to an enhanced ability of the combination treatment to inhibit certain cancer cell phenotypes. We found this to be true in this investigation.”

A 2008 scientific review published in the journal Cancer Research reported that the cannabinioids inhibit cell proliferation in a wide range of cancers, including brain cancer, prostate cancer, breast cancer, lung cancer, skin cancer, pancreatic cancer, and lymphoma.”

http://norml.org/news/2010/01/21/marijuana-compounds-possess-synergistic-anti-cancer-effects-study-says