A double-blind, randomized, placebo-controlled, parallel group study of THC/CBD spray in peripheral neuropathic pain treatment.

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“Peripheral neuropathic pain (PNP) associated with allodynia poses a significant clinical challenge. The efficacy of Δ9 -tetrahydrocannabinol/cannabidiol (THC/CBD) oromucosal spray, a novel cannabinoid formulation, was investigated in this 15-week randomized, double-blind, placebo-controlled parallel group study…

These findings demonstrate that, in a meaningful proportion of otherwise treatment-resistant patients, clinically important improvements in pain, sleep quality and SGIC of the severity of their condition are obtained with THC/CBD spray. THC/CBD spray was well tolerated and no new safety concerns were identified.”

http://www.ncbi.nlm.nih.gov/pubmed/24420962

The endocannabinoid system: an emerging key player in inflammation.

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“The purpose of this review is to illustrate the expanding view of the endocannabinoid system (ECS) in relation to its roles in inflammation…

Diet is among the main factors determining synthesis and release of endocannabinoids and related mediators.

SUMMARY:

The complexity of what may be called the ‘endocannabinoidome’ requires approaches that take into account its dynamics and interconnections with other regulatory systems. This endocannabinoidome continues to offer possibilities for prevention and intervention, but multiple target approaches will probably provide the only keys to success.”

http://www.ncbi.nlm.nih.gov/pubmed/24419242

Pharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat.

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“Addiction to major drugs of abuse, such as cocaine, has recently been linked to alterations in adult neurogenesis in the hippocampus. The endogenous cannabinoid system modulates this proliferative response as demonstrated by the finding that pharmacological activation/blockade of cannabinoid CB1 and CB2 receptors not only modulates neurogenesis but also modulates cell death in the brain.

In the present study, we evaluated whether the endogenous cannabinoid system affects cocaine-induced alterations in cell proliferation…

These results indicate that the changes in neurogenic, apoptotic and gliotic processes that were produced by repeated cocaine administration were normalized by pharmacological blockade of CB1 and CB2. The restorative effects of cannabinoid receptor blockade on hippocampal cell proliferation were associated with the prevention of the induction of conditioned locomotion but not with the prevention of cocaine-induced sensitization.”

http://www.ncbi.nlm.nih.gov/pubmed/24409127

CB2 Receptor Deficiency Increases Amyloid Pathology and Alters Tau Processing in a Transgenic Mouse Model of Alzheimer’s Disease.

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“The endocannabinoid CB2 receptor system has been implicated in the neuropathology of Alzheimer’s disease (AD)…

The results confirm the constitutive role of the CB2 receptor system both in reducing amyloid plaque pathology in AD and also support the potential of cannabinoid therapies targeting CB2 to reduce Aβ…”

http://www.ncbi.nlm.nih.gov/pubmed/24408112

Modulation of Gut-Specific Mechanisms by Chronic Δ9-THC Administration in Male Rhesus Macaques Infected with Simian Immunodeficiency Virus: A Systems Biology Analysis.

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“Our studies have demonstrated that chronic Δ9-tetrahydrocannabinol (THC) administration results in a generalized attenuation of viral load and tissue inflammation in simian immunodeficiency virus (SIV)-infected male rhesus macaques…

Our results indicate that chronic THC treatment modulated duodenal T cell populations, favored a pro-Th2 cytokine balance, and decreased intestinal apoptosis.

These findings reveal novel mechanisms that may potentially contribute to cannabinoid-mediated disease modulation.”

http://www.ncbi.nlm.nih.gov/pubmed/24400995

“Previous studies from our laboratory have shown that chronic THC administration ameliorates SIV disease progression and significantly reduces the morbidity and mortality of male SIV-infected macaques… In summary, using a systems biology approach to understanding the impact of chronic cannabinoid treatment on gut-associated immunopathology, we identified relevant mechanisms that can potentially modulate disease progression. Our results suggest that gut immunomodulation through changes in gene expression, cytokine profiles, and immune cell populations could potentially contribute to chronic THC modulation of SIV disease progression. Moreover, they reveal novel mechanisms that may potentially contribute to decreased morbidity and mortality.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046212/

Acute alcohol use temporally increases the odds of male perpetrated dating violence: A 90-day diary analysis.

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“…the present study examined the temporal relationship between acute alcohol use, marijuana use, and male perpetrated physical, psychological, and sexual dating violence…

On any alcohol use days, heavy alcohol use days (5 or more standard drinks), and as the number of drinks increased on a given day, the odds of physical and sexual aggression perpetration increased. The odds of psychological aggression increased on heavy alcohol use days only.

Marijuana use days did not increase the odds of any type of aggression.

CONCLUSIONS:

These findings contribute to a growing body of research on the temporal relation between acute alcohol use and IPV perpetration among college men. Combined with previous research, our findings suggest that dating violence intervention and prevention programs should target reductions in alcohol use.”

http://www.ncbi.nlm.nih.gov/pubmed/24199932

Cannabidiol protects liver from binge alcohol-induced steatosis by mechanisms including inhibition of oxidative stress and increasing of autophagy.

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“Acute alcohol drinking induces steatosis, and effective prevention of steatosis can protect liver from progressive damage caused by alcohol… We evaluated whether cannabidiol, which has been reported to function as an antioxidant, can protect the liver from alcohol-generated oxidative stress induced steatosis.

Cannabidiol can prevent acute alcohol induced liver steatosis in mice… Importantly, cannabidiol can prevent the decrease of autophagy induced by alcohol.

In conclusion, these results show that cannabidiol protects mouse liver from acute alcohol induced steatosis through multiple mechanisms including attenuation of alcohol-mediated oxidative stress, prevention of JNK MAPK activation, and increasing autophagy.”

http://www.ncbi.nlm.nih.gov/pubmed/24398069

Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far

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“Emerging findings suggest the existence of a cross-talk between hypocretinergic and endocannabinoid systems…

The present review attempts to piece together what is known about this interesting interaction and describes its potential therapeutic implications.”

http://www.frontiersin.org/Neuropharmacology/10.3389/fnins.2013.00256/abstract

Clinical experience with THC:CBD oromucosal spray in patients with multiple sclerosis-related spasticity.

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“This detailed medical charts’ data collection study conducted at an MS clinic in Germany evaluated the effectiveness of tetrahydrocannabinol (THC) / cannabidiol (CBD) oromucosal spray in patients with resistant multiple sclerosis (MS) spasticity…

In this routine clinical practice setting at an MS clinic in Germany, THC:CBD spray was effective and well tolerated as add-on therapy or as monotherapy in a relevant proportion of patients with resistant MS spasticity.”

http://www.ncbi.nlm.nih.gov/pubmed/24392812

Association between a Genetic Variant of Type-1 Cannabinoid Receptor and Inflammatory Neurodegeneration in Multiple Sclerosis

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“Genetic ablation of type-1 cannabinoid receptors (CB1Rs) exacerbates the neurodegenerative damage of experimental autoimmune encephalomyelitis, the rodent model of multiple sclerosis (MS)…

Our results demonstrate the biological relevance of the (AAT)n CNR1 repeats in the inflammatory neurodegenerative damage of MS…

In conclusion, our study points to CB1R as an interesting molecular target for preventing neuronal loss and cognitive impairment in MS as well as in other CNS disorders in which inflammation-driven neurodegeneration process play a role.”

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0082848