“Cannabisol (1), a unique dimer of Δ9-tetrahydrocannabinol (Δ9-THC) with a methylene bridge, was isolated from Cannabis sativa.
This is the first example of a C-bridged dimeric cannabinoid.
The structure of 1 was unambiguously deduced by HRESIMS, GCMS, and NMR spectroscopy.
A plausible biogenesis of 1 is described.”
“Recent clinical and preclinical research has suggested that cannabidiol (CBD) and Δ9-tetrahydrocannabinol (Δ9-THC) have interactive effects on measures of cognition; however, the nature of these interactions is not yet fully characterized.
To address this, we investigated the effects of Δ9-THC and CBD independently and in combination with proposed therapeutic dose ratios of 1:1 and 1:3 Δ9-THC:CBD in adult rhesus monkeys performing a stop signal task (SST).
These results indicate that CBD, when combined with Δ9-THC in clinically available dose ratios, does not exacerbate and, under restricted conditions may even attenuate, Δ9-THC’s behavioral effects.”
“Patients recovered from Ebola virus infection may experience short- and long-term physical, neuropsychological and social sequelae, including arthralgia, musculoskeletal pain, ophthalmic inflammation, auditory problems, fatigue, confusion, insomnia, short-term memory impairment, anxiety, depression and anorexia, all lasting from 2 weeks to more than 2 years.
Currently there are no treatments for post Ebola sequelae.
We hypothesize that cannabidiol (CBD) may attenuate some of these post Ebola sequelae, several of which have been postulated to result from inflammation and/or an autoimmune response.
CBD has anti-inflammatory actions in various animal models.
Clinical studies have shown that oral administration of CBD, compared to placebo, significantly reduces anxiety, has antinociceptive and anticonvulsant actions, and may be therapeutic for insomnia.
Overall, CBD has a number of pharmacological effects that may significantly improve the mental and somatic health of patients suffering from post Ebola sequelae.
In humans, CBD, at therapeutic doses, does not: 1) elicit dependence or tolerance; 2) significantly alter heart rate or blood pressure; 3) affect gastrointestinal transit; 4) produce significant cognitive or psychomotor impairments. Mild sedation and nausea are the most commonly reported adverse effects associated with CBD.
CBD, based on its pharmacological effects and favorable safety profile, should be considered as a treatment for individuals with post Ebola sequelae.”
https://www.ncbi.nlm.nih.gov/pubmed/27686726
“The use of cannabidiol (CBD) to treat post Ebola clinical sequelae is proposed. CBD could decrease pain, inflammation, and neuropsychological problems. CBD does not elicit significant adverse or toxic effects in humans.”
“In conclusion, it is hypothesized that CBD, based on its pharmacological effects and favorable safety profile, should be considered as a treatment for individuals with post Ebola syndrome.”
https://www.ijidonline.com/article/S1201-9712(16)31177-8/fulltext
“To test the neuroprotective effects of the nonpsychoactive cannabinoid cannabidiol (CBD), piglets received i.v. CBD or vehicle after hypoxia-ischemia (HI: temporary occlusion of both carotid arteries plus hypoxia).
CBD administration was free from side effects; moreover, CBD administration was associated with cardiac, hemodynamic, and ventilatory beneficial effects.
In conclusion, administration of CBD after HI reduced short-term brain damage and was associated with extracerebral benefits.”
“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 the brain, there were fewer normal and more pyknotic neurons, while astrocytes were less numerous and swollen. Cerebrospinal fluid concentration of neuronal-specific enolase (NSE) and S100β protein and brain tissue percentage of TNFα(+) cells were all higher. In contrast, in HI + CBD, aEEG had recovered to 86 ± 5%, NIRS parameters increased, and the neurobehavioral score normalized (34.3 ± 1.4 points). HI induced histological changes, and NSE and S100β concentration and TNFα(+) cell increases were suppressed by CBD. In conclusion, post-HI administration of CBD protects neurons and astrocytes, leading to histological, functional, biochemical, and neurobehavioral improvements.”
“Cannabidiol (CBD) demonstrated short-term neuroprotective effects in the immature brain following hypoxia-ischemia (HI).
We examined whether CBD neuroprotection is sustained over a prolonged period.
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.
These effects of CBD were not associated with any side effects.
These results emphasize the interest in CBD as a neuroprotective agent for neonatal HI.”
“A relevant therapeutic time window (TTW) is an important criterion for considering the clinical relevance of a substance preventing newborn hypoxic-ischemic (HI) brain damage.
to test the TTW of the neuroprotective effects of cannabidol (CBD), a non-psychoactive cannabinoid in a model of newborn HI brain damage.
CBD administered up to 18 h after HI reduced IHVL and neuropathological score by 60%, TUNEL+ count by 90% and astrocyte damage by 50%. In addition, CBD blunted the HI-induced increase in microglial population. When CBD administration was delayed 24 h, however, the neuroprotective effect was lost in terms of IHVL, apoptosis or astrogliosis reduction.
CBD shows a TTW of 18 h when administered to HI newborn mice, which represents a broader TTW than reported for other neuroprotective treatments including hypothermia.”
“Aging-related neurodegenerative diseases, such as Parkinson’s disease (PD) or related disorders, are an increasing societal and economic burden worldwide.
Δ9-Tetrahydrocannabinol (THC) is discussed as a neuroprotective agent in several in vitro and in vivo models of brain injury. However, the mechanisms by which THC exhibits neuroprotective properties are not completely understood.
In the present study, we investigated neuroprotective mechanisms of THC in glutamate-induced neurotoxicity in primary murine mesencephalic cultures, as a culture model for PD.
THC protected dopaminergic neurons and other cell types of primary dissociated cultures from glutamate-induced neurotoxicity.
Moreover, THC significantly counteracted the glutamate-induced mitochondrial membrane depolarization and apoptosis.
In conclusion, THC exerts anti-apoptotic and restores mitochondrial membrane potential via a mechanism dependent on CB1 receptor.
It strengthens the fact that THC has a benefit on degenerative cellular processes occurring, among others, in PD and other neurodegenerative diseases by slowing down the progression of neuronal cell death.”
https://www.ncbi.nlm.nih.gov/pubmed/27654887
http://onlinelibrary.wiley.com/wol1/doi/10.1002/ptr.5712/full
“Schizophrenia is a severe psychiatric disorder that involves positive, negative and cognitive symptoms. Prepulse inhibition of startle reflex (PPI) is a paradigm that assesses the sensorimotor gating functioning and is impaired in schizophrenia patients as well as in animal models of this disorder. Recent data point to the participation of the endocannabinoid system in the pathophysiology and pharmacotherapy of schizophrenia. Here, we focus on the effects of cannabinoid drugs on the PPI deficit of animal models of schizophrenia, with greater focus on the SHR (Spontaneously Hypertensive Rats) strain, and on the future prospects resulting from these findings.”
“Cannabis is the most popular illicit drug on the European market. Over 16 million young Europeans have used it at least once in the last few years. The recent trends in the consumption of marihuana differ between countries. Some countries face an increase in the prevalence of cannabis use, including Poland, where the level cannabis use has been systematically increasing since the 1990’s. According to a recent ESPAD study, 19% of Polish adolescents aged 15-16 have used cannabis in the last year. Marihuana is also a leading substance when analyzing the data of seizures and crimes. The recent EMCDDA Annual report on the drug situation in Europe notes the increasing potency in cannabis available on the market. Some countries face an increasing number of emergencies caused by marihuana, which was unlikely to have happened previously. In almost all European countries there is an ongoing discussion about loosening marijuana laws or its complete legalization. There is also ongoing discussion on the use of marihuana in therapy as a medicine. Many scientific studies are being conducted in this field. Some of the results are promising; however, there is no well-designed human trial which would unequivocally confirm that medical cannabis is effective as a medicine, or more effective than other medicines on the market. The problem is that the debate on the medical use of marihuana becomes more ideological and less professional. The medical use of marihuana is strongly supported by organizations lobbying for the legalization of cannabis use. Research on the medical use of cannabis should be continued, as there are some promising results supporting therapy in different medical conditions. However, the use of cannabis as a medicine should be discussed only among professionals. If marihuana is to be used for medical purposes, the fact that it is the most popular illicit drug in Europe is irrelevant.”
