Newly Released Studies Show Protection and Regeneration of Brain Cells with Cannabis Therapies

There are over 1.7 million cases of severe brain injury that are reported each year.  These injuries can be life altering for many but thanks to the hard work from the science and medical communities we are learning more about new treatment options.  Cannabis has been discovered to help with cell regeneration and repair in the brain.  Below you will see newly published studies where  cannabis has been applied to help with brain injuries. Truly exciting!!   As always I encourage all to do their own research as well and please feel free to share ~ Cherry Girl

Early Survival of Comatose Patients After Severe Traumatic Brain Injury With the Dual Cannabinoid CB1/CB2 Receptor Agonist KN38-7271
Despite many drug trials, no substance has yet been identified that improves the outcome of severe head injury. The dual cannabinoid CB1/CB2 receptor agonist KN38-7271 mediates potent neuroprotection in animal models. We describe here the first randomized, double-blind, prospective, placebo-controlled clinical phase IIa proof-of-concept trial to investigate the safety, pharmacokinetics, and potential efficacy of a cannabinoid receptor agonist in humans.  Conclusions KN38-7271 appeared beneficial in the acute early phase of the comatose patient after a head injury. Its use was safe and well tolerated by patients.

Cannabinoids As Neuroprotective Agents In Traumatic Brain Injury
Cannabinoids of all classes have the ability to protect neurons from a variety of insults that are believed to underlie delayed neuronal death after traumatic brain injury (TBI), including excitotoxicity, calcium influx, free radical formation and neuroinflammation.

Cannabidiol Administration After Hypoxia-Ischemia To Newborn Rats Reduces Long-Term Brain Injury and Restores Neurobehavioral Function 2012
Cannabidiol (CBD) demonstrated short-term neuroprotective effects in the immature brain following hypoxia-ischemia (HI).   In conclusion, CBD administration after HI injury to newborn rats led to long-lasting neuroprotection, with the overall effect of promoting greater functional rather than histological recovery.

Cannabidiol Reduces Brain Damage and Improves Functional Recovery After Acute Hypoxia-Ischemia In Newborn Pigs 2011
Newborn piglets exposed to acute hypoxia-ischemia (HI) received i.v. cannabidiol (HI + CBD) or vehicle (HI + VEH). In HI + VEH, 72 h post-HI brain activity as assessed by amplitude-integrated EEG (aEEG) had only recovered to 42 ± 9% of baseline, near-infrared spectroscopy (NIRS) parameters remained lower than normal, and neurobehavioral performance was abnormal (27.8 ± 2.3 points, normal 36).   In conclusion, post-HI administration of CBD protects neurons and astrocytes, leading to histological, functional, biochemical, and neurobehavioral improvements.
 

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How Some Green Can Help The Blues

Americans across the nation are facing mounting pressure from the economy and many other challenges.  Many are also suffering with depression and mood disorders along with added pressures.  The average American who has tried cannabis well knows the mood elevating effects which include uncontrollable giggling or laughter.  Of course it is also dependent on the right strain but that is where science comes in.  Below you will see studies where scientists have discovered why our moods are altered as well as further the knowledge we have on the interactions of cannabis’ compounds and our bodies.  Please feel free to share and I encourage all to do their own research as well ~ Cherry Girl

The Dopamine and Cannabinoid Interaction in the Modulation of Emotions and Cognition: Assessing the Role of Cannabinoid CB1 Receptor in Neurons Expressing Dopamine D1 Receptors
Although cannabinoid CB1 receptors (CB1Rs) are densely expressed in neurons expressing dopamine D1 receptors (D1Rs), it is not fully understood to what extent they modulate emotional behaviors…….These results provided first direct evidence for a cross-talk between dopaminergic D1Rs and endocannabinoid system in terms of controlling negative affect.

Effects of Cannabinoids Δ(9)-tetrahydrocannabinol, Δ(9)-tetrahydrocannabinolic Acid and Cannabidiol in MPP(+) Affected Murine Mesencephalic Cultures
Cannabinoids derived from Cannabis sativa demonstrate neuroprotective properties… Therefore we studied some major cannabinoids, i.e. delta-9-tetrahydrocannabinolic acid (THCA), delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) in mice mesencephalic cultures for their protective capacities… our data show that cannabinoids THC and THCA protect dopaminergic neurons against MPP(+) induced cell death.” (Possibly due to the cross-talk between  the dopamine and cannabinoid systems as seen in the study above)

Antidepressant-like Effect of Δ9-tetrahydrocannabinol and Other Cannabinoids Isolated From Cannabis
Results of this study show that Δ9-THC and other cannabinoids exert antidepressant-like actions, and thus may contribute to the overall mood-elevating properties of cannabis.

 

Cannabis and Brain Disorders: Cannabinoids Targeting the Endocannabinoid System and Receptors As A Means to CURE

Below are studies that show how cannabis affects the central nervous system.  These studies suggest that cannabis can aid in treating brain disorders.  With more research we can prove that marijuana does have medicinal value and can greatly aid or cure many ailments.  These are published medical studies that I encourage you to research and share your findings with everyone.  Spread the truth!
Information gathered by David Worrell edited by Cherry Girl

It is not important that you fully understand all the scientific mumbo-jumbo. What is important, what you need to understand, is that there are “Functional Neuronal CB2 Cannabinoid Receptors in the Central Nervous System”  ~ D.W.

Functional Neuronal CB2 Cannabinoid Receptors in the Central Nervous System
“Cannabinoids are the constituents of the marijuana plant (Cannabis sativa). The recent progress in marijuana-cannabinoid research include the discovery of an endocannabinoid system with specific genes coding for cannabinoid receptors (CBRs) that are activated by smoking marijuana, and that the human body and brain makes its own marijuana-like substances called endocannabinoids that also activate CBRs.”
‎”Commentary: Functional Neuronal CB2 Cannabinoid Receptors in the CNS.
Onaivi ES.  SourceWilliam Paterson University, Wayne NJ and Molecular Neurobiology Branch, National Institute on Drug Abuse, NIH, Baltimore, USA.

Abstract
Cannabinoids are the constituents of the marijuana plant (Cannabis sativa). There are numerous cannabinoids and other natural compounds that have been reported in the cannabis plant. The recent progress in marijuana-cannabinoid research include the discovery of an endocannabinoid system with specific genes coding for cannabinoid receptors (CBRs) that are activated by smoking marijuana, and that the human body and brain makes its own marijuana-like substances called endocannabinoids that also activate CBRs. This new knowledge and progress about cannabinoids and endocannabinoids indicate that a balanced level of endocannabinoids is important for pregnancy and that the breast milk in animals and humans has endocannabinoids for the growth and development of the new born. There are two well characterized cannabinoid receptors termed CB1-Rs and CB2-Rs and these CBRs are perhaps the most abundant G-protein coupled receptors that are expressed at high levels in many regions of the mammalian brain. The expression of CB1-Rs in the brain and periphery and the identification of CB2-Rs in immune cells and during inflammation has been extensively studied and characterized. However, the expression of functional neuronal CB2-Rs in the CNS has been much less well established and characterized in comparison to the expression of abundant brain CB1-Rs and functional neuronal CB2-Rs has ignited debate and controversy. While the issue of the specificity of CB2-R antibodies remains, many recent studies have reported the discovery and functional characterization of functional neuronal CB2-Rs in the CNS beyond neuro-immuno cannabinoid activity.”   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137183/?tool=pubmed


Targeting the Endocannabinoid System in Treating Brain Disorders.
“Many studies on cannabinoids indicate important progress for protection against several neurodegenerative disorders.This review highlights recent studies implicating the endocannabinoid system in neuroprotection against different disorders of the CNS.” (Central Nervous System)
‎”Targeting the endocannabinoid system in treating brain disorders.Bahr BA, Karanian DA, Makanji SS, Makriyannis A. SourceDepartment of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06269, USA. Bahr@uconn.edu

Abstract
Recent cannabinoid research has a primary focus on developing therapeutics against human diseases. Many studies on Cannabinoids indicate important progress for protection against several Neurodegenerative disorders.  Agonists of cannabinoid receptors activate signalling pathways in the brain that are linked to neuronal repair and cell maintenance, and endogenous ligands can also activate neuroprotective responses. These endocannabinoids are bioactive fatty acid amides and esters that are synthesised in the brain and include arachidonoyl ethanolamide (anandamide) and 2-arachidonoyl glycerol. Endocannabinoids are released in response to pathogenic events, thus representing a potential compensatory repair mechanism. Enhancing this on-demand action of endocannabinoids is a strategy with which to promote endogenous repair signalling. For such enhancement, considerable work has gone into modulating the availability of endocannabinoids by blocking the processes of their deactivation. The targets include the anandamide-hydrolysing enzyme fatty acid amide hydrolase, the carrier-mediated anandamide transport system and 2-arachidonoyl glycerol-deactivating enzyme monoacylglycerol lipase. The activity of endocannabinoids is terminated through transport and degradation and, accordingly, selective inhibitors of these processes effectively exploit the protective nature of cannabinergic responses. This review highlights recent studies implicating the endocannabinoid system in neuroprotection against different disorders of the Central Nervous System.”  http://www.ncbi.nlm.nih.gov/pubmed/16548785

Cannabinoids: A New Group of Agonists of PPARs
Cannabinoids have been used medicinally for thousands of years. In preclinical studies cannabinoids displayed many of the characteristics of nonsteroidal anti-inflammatory drugs (NSAIDs) and seem to be free of unwanted side effects. An increasing number of therapeutic actions of cannabinoids are being reported…
Sun Y, Bennett A.  SourceSchool of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK. stxys3@nottingham.ac.uk

Abstract
Cannabinoids have been used medicinally and recreationally for thousands of years and their effects were proposed to occur mainly via activation of the G-protein-coupled receptor CB1/CB2 (cannabinoid receptor 1/2). Discovery of potent synthetic analogs of the natural cannabinoids as clinically useful drugs is the sustained aim of cannabinoid research. This demands that these new compounds be free of the psychotropic effects that connected with the recreational use of cannabinoids. In preclinical studies cannabinoids displayed many of the characteristics of nonsteroidal anti-inflammatory drugs (NSAIDs) and it seems to be free of unwanted side effects. An increasing number of therapeutic actions of cannabinoid are being reported that do not appear to be mediated by either CB1 or CB2, and recently nuclear receptor superfamily PPARs (peroxisome-proliferator-activated receptors) have been suggested as the target of certain cannabinoids. This review summarizes the evidence for cannabinoid activation on PPARs and possible associated remedial potentials.”
‎”In summary, there is strong evidence to suggest that some cannabinoids can act on PPARs through either direct or indirect pathways. These discoveries not only broaden the promising usage of cannabinoids as therapeutic agents, but also support PPARs as new targets for some neuroprotective treatment.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2220031/?tool=pubmed

Cannabinoid Activation of PPARα; A Novel Neuroprotective Mechanism
“Conclusions and implications:These data demonstrate the potential for a range of cannabinoid compounds, of diverse structures, to activate PPAR alpha and suggest that at least some of the neuroprotective properties of these agents could be mediated by nuclear receptor activation.”
‎”Cannabinoid activation of PPAR alpha; a novel neuroprotective mechanism.
Sun Y, Alexander SP, Garle MJ, Gibson CL, Hewitt K, Murphy SP, Kendall DA, Bennett AJ.
SourceSchool of Biomedical Sciences, University of Nottingham Medical School, Nottingham, UK.

Abstract
BACKGROUND AND PURPOSE: Although CB(1) receptor activation evokes neuroprotection in response to cannabinoids, some cannabinoids have been reported to be peroxisome proliferator activated receptor (PPAR) ligands, offering an alternative protective mechanism. We have, therefore, investigated the ability of a range of cannabinoids to activate PPAR alpha and for N-oleoylethanolamine (OEA), an endogenous cannabinoid-like compound (ECL), to evoke neuroprotection.

EXPERIMENTAL APPROACH:
Assays of PPAR alpha occupancy and gene transactivation potential were conducted in cell-free and transfected HeLa cell preparations, respectively. In vivo estimates of PPAR alpha activation through fat mobilization and gene transcription were conducted in mice. Neuroprotection in vivo was investigated in wild-type and PPAR alpha gene-disrupted mice.

KEY RESULTS: The ECLs OEA, anandamide, noladin ether and virodhamine were found to bind to the purified PPAR alpha ligand binding domain and to increase PPAR alpha-driven transcriptional activity. The high affinity synthetic CB(1/2) cannabinoid agonist WIN 55212-2 bound to PPAR alpha equipotently with the PPARalpha agonist fenofibrate, and stimulated PPARalpha-mediated gene transcription. The phytocannabinoid delta 9 tetrahydrocannabinol was without effect. OEA and WIN 55212-2 induced lipolysis in vivo, while OEA pre-treatment reduced infarct volume from middle cerebral artery occlusion in wild-type, but not in PPAR alpha-null mice. OEA treatment also led to increased expression of the NFkappa B-inhibitory protein, Ikappa B, in mouse cerebral cortex, while expression of the NFkappa B-regulated protein COX-2 was inhibited. Conclusions and implications:These data demonstrate the potential for a range of cannabinoid compounds, of diverse structures, to activate PPAR alpha and suggest that at least some of the neuroprotective properties of these agents could be mediated by nuclear receptor activation.”

‎”In summary, the data presented here provide strong evidence that selected cannabinoids (WIN 55212-2, OEA, noladin ether and virodhamine) are PPARα agonists, and suggest a novel means by which the multiple effects of cannabinoids, in boththe CNS and periphery, could be brought about. In addition to its well-recognized role in lipid metabolism, PPARα activation showed obvious beneficial effects in ischaemic brain damage, which is likely to be connected with its anti-inflammatory action through the NF–κB pathway. These discoveries not only broaden the potential use of cannabinoids as therapeutic agents, but also support PPARα as a new target for neuroprotectiv treatment.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190030/?tool=pubmed


Cannabinoids and PPARalpha Signalling

“Cannabinoids have been shown to possess anti-inflammatory and neuroprotective properties.This review summarizes the evidence for cannabinoid activation of PPARs and identifies a new intracellular target for cannabinoids as therapeutic agents for neuroprotective treatment.”
‎”Cannabinoids and PPARalpha signalling. Sun Y, Alexander SP, Kendall DA, Bennett AJ. SourceSchool of Biomedical Sciences, University of Nottingham, Nottingham NG7 2UH, UK. stxys3@nottingham.ac.uk

Abstract
Cannabinoids have been shown to possess anti-inflammatory and neuroprotective properties, which were proposed to occur mainly via activation of the G-protein-coupled receptor CB(1) (cannabinoid receptor 1). Recently, certain cannabinoids have been reported to be ligands for members of the nuclear receptor transcription factor superfamily known as PPARs (peroxisome-proliferator-activated receptors). This review summarizes the evidence for cannabinoid activation of PPARs and identifies a new intracellular target for cannabinoids as therapeutic agents for neuroprotective treatment.”
http://www.ncbi.nlm.nih.gov/pubmed/17073758