“This is an exciting time for cannabinoid research. The discovery of cannabinoid CB1receptors (expressed by central and peripheral neurones) and CB2 receptors (expressed mainly by immune cells) and endogenous agonists for these receptors has renewed the scientific community’s interest. Independently of these developments society at large has continued an aggressive debate about the therapeutic use of cannabinoids, including demands for their more liberal availability. Cannabinoids have been suggested to have therapeutic value as analgesics and in various conditions, including migraine headaches, nausea and vomiting, wasting syndrome and appetite stimulation in HIV-infected patients, muscle spasticity due to multiple sclerosis or spinal cord injury, movement disorders such as Parkinson’s disease, epilepsy, and glaucoma.”
Monthly Archives: April 2014
Memory Loss From Marijuana Blocked By Ibuprofen; Drug Duo May Halt Alzheimer’s Progression
“Marijuana’s primary side-effect as a medicine — memory loss — may soon become all but forgotten.
In a stunningly simple turn, investigators found that a simple over-the-counter painkiller, such as ibuprofen, blocks memory loss from the drug’s active ingredient, delta-9-tetrahydrocannabinol (THC). The drug combination may also prevent neurological damage from Alzheimer’s Disease, opening possibilities too for the treatment of a variety of other diseases and conditions.
Nearly five millennia into the history of medical marijuana, investigators from Louisiana State University Health Sciences Center say they’ve found a way to strip marijuana’s most deleterious side effect. The discovery may prompt U.S. regulators to soon approve marijuana-based treatments for ailments beyond nausea and vomiting in chemotherapy patients.”
Targeting the endocannabinoid system in the treatment of fragile X syndrome.
“Fragile X syndrome (FXS), the most common monogenic cause of inherited intellectual disability and autism, is caused by the silencing of the FMR1 gene, leading to the loss of fragile X mental retardation protein (FMRP), a synaptically expressed RNA-binding protein regulating translation.
The endocannabinoid system (ECS) is a key modulator of synaptic plasticity, cognitive performance, anxiety, nociception and seizure susceptibility, all of which are affected in FXS. The cannabinoid receptors CB1 (CB1R) and CB2 (CB2R) are activated by phospholipid-derived endocannabinoids, and CB1R-driven long-term regulation of synaptic strength, as a consequence of mGluR5 activation, is altered in several brain areas of Fmr1 knockout mice.
We found that CB1R blockade in male Fmr1 knockout (Fmr1(-/y)) mice through pharmacological and genetic approaches normalized cognitive impairment, nociceptive desensitization, susceptibility to audiogenic seizures, overactivated mTOR signaling and altered spine morphology, whereas pharmacological blockade of CB2R normalized anxiolytic-like behavior. Some of these traits were also reversed by pharmacological inhibition of mTOR or mGluR5.
Thus, blockade of ECS is a potential therapeutic approach to normalize specific alterations in FXS.”
Role of the cannabinoid system in the transit of beta-amyloid across the blood-brain barrier.
“Emerging evidence suggests beta-amyloid (Aβ) deposition in the Alzheimer’s disease (AD) brain is the result of impaired clearance, due in part to diminished Aβ transport across the blood-brain barrier (BBB). Recently, modulation of the cannabinoid system was shown to reduce Aβ brain levels and improve cognitive behavior in AD animal models.
The purpose of the current studies was to investigate the role of the cannabinoid system in the clearance of Aβ across the BBB..
The current studies demonstrate, for the first time, a role for the cannabinoid system in the transit of Aβ across the BBB. These findings provide insight into the mechanism by which cannabinoid treatment reduces Aβ burden in the AD brain and offer additional evidence on the utility of this pathway as a treatment for AD.”
http://www.ncbi.nlm.nih.gov/pubmed/23831388
http://www.thctotalhealthcare.com/category/alzheimers-disease-ad/
Marijuana may help prevent Alzheimer’s, but research hits dead end
“Early use of marijuana might forestall the onset of Alzheimer’s and improve memory in old people, says Gary Wenk, a long-time researcher whose work with marijuana and this disease has come to halt.
“We found out that people who smoked dope in the 1960s were not getting Alzheimer’s,” Wenk said. “These 90-year-olds without dementia were telling us things like, ‘Well, I drank whiskey and smoked dope,’ and these are the things they remember. They don’t remember habits like how often they ate broccoli.”
But lately, due to political, legal and financial reasons, his research progress have come to a halt.
“The evidence in animals is clear but making the leap to humans mean that you have to find a drug company willing to handle the lawsuits and the money,” Wenk said.”
http://www.thctotalhealthcare.com/category/alzheimers-disease-ad/
Multitarget cannabinoids as novel strategy for Alzheimer disease.
“During the last years the development of approaches to multitarget drug design and discovery is gaining acceptance. The cannabinoids are potentially excellent multi-target drug candidates because of their interesting pharmacological profiles, among which stands out the dual capacity of cannabinoid ligands to act as cannabinoid agonist and cholinesterase inhibitors.”
http://www.ncbi.nlm.nih.gov/pubmed/23369066
http://www.thctotalhealthcare.com/category/alzheimers-disease-ad/
The Effect of Medical Marijuana Laws on Crime: Evidence from State Panel Data, 1990-2006
“Debate has surrounded the legalization of marijuana for medical purposes for decades. Some have argued medical marijuana legalization (MML) poses a threat to public health and safety, perhaps also affecting crime rates. In recent years, some U.S. states have legalized marijuana for medical purposes, reigniting political and public interest in the impact of marijuana legalization on a range of outcomes.
Relying on U.S. state panel data, we analyzed the association between state MML and state crime rates for all Part I offenses collected by the FBI.
Results did not indicate a crime exacerbating effect of MML on any of the Part I offenses. Alternatively, state MML may be correlated with a reduction in homicide and assault rates, net of other covariates.
“No correlation between medical marijuana legalization, crime increase: Legalization may reduce homicide, assault rates” http://www.sciencedaily.com/releases/2014/03/140326182049.htm
“Medical Marijuana’s Legalization Doesn’t Raise Crime Rates: Study” http://consumer.healthday.com/mental-health-information-25/behavior-health-news-56/briefs-emb-3-26-5pmet-medical-pot-crime-plos-one-utd-release-batch-1198-686131.html
“Legalization of medical marijuana does not lead to increased crime, and may even be tied to lower rates of offenses such as assault and murder, a new study suggests.” http://www.webmd.com/pain-management/news/20140326/medical-marijuanas-legalization-doesnt-raise-crime-rates-study
“Marijuana use reduces violent crime: Study” http://timesofindia.indiatimes.com/india/Marijuana-use-reduces-violent-crime-Study/articleshow/32777752.cms
“No, legalizing medical marijuana doesn’t lead to crime, according to actual crime stats…In fact, states that have legalized it appear to have seen some reductions in the rates of homicide and assault.” http://www.washingtonpost.com/blogs/wonkblog/wp/2014/03/26/no-legalizing-medical-marijuana-doesnt-lead-to-crime-according-to-actual-crime-stats/?tid=pm_business_pop
Delta-9-Tetrahydrocannabinol/Cannabidiol (Sativex®): A Review of Its Use in Patients with Moderate to Severe Spasticity Due to Multiple Sclerosis.
“Delta-9-tetrahydrocannabinol (THC)/cannabidiol (CBD) [Sativex®] is an oromucosal spray formulation that contains principally THC and CBD at an approximately 1:1 fixed ratio, derived from cloned Cannabis sativa L. plants.
The main active substance, THC, acts as a partial agonist at human cannabinoid receptors (CB1 and CB2)…
THC/CBD is approved in a number of countries, including Germany and the UK, as an add-on treatment for symptom improvement in adult patients with moderate to severe spasticity due to multiple sclerosis who have not responded adequately to other anti-spasticity medication and who demonstrate clinically significant improvement in spasticity-related symptoms during an initial trial of therapy.
In the largest multinational clinical trial that evaluated the approved THC/CBD regimen in this population, 12 weeks’ double-blind treatment with THC/CBD significantly reduced spasticity severity (primary endpoint) compared with placebo in patients who achieved a clinically significant improvement in spasticity after 4 weeks’ single-blind THC/CBD treatment, as assessed by a patient-rated numerical rating scale.
A significantly greater proportion of THC/CBD than placebo recipients achieved a ≥30 % reduction (a clinically relevant reduction) in spasticity severity. The efficacy of THC/CBD has been also shown in at least one everyday clinical practice study (MOVE 2). THC/CBD was generally well tolerated in clinical trials. Dizziness and fatigue were reported most frequently during the first 4 weeks of treatment and resolved within a few days even with continued treatment.
Thus, add-on THC/CBD is a useful symptomatic treatment option for its approved indication.”