CBD is a compound in cannabis mostly associated with therapeutic effects. We take a look at how it impacts the brain. The unique effects of CBD in the brain are key to its immense healing potential. In this piece, we take a deep dive into the latest science on the. The dose of THC the brain required in order to experience a typical “high” is a Animal studies have discovered many beneficial effects of CBD but only when.
effects on brain cannabidiol the
When low energy is an issue, sativa or other stimulating strains can be helpful for improving energy and focus when THC can be tolerated. Varieties that are high in the terpene limonene are recommended for mood elevation. Always start with the micro dose to test sensitivity and go up as needed within the dosing range before going to the next, until symptoms subside. The micro to standard dose is usually recommended to treat depression.
Vaporized or smoked cannabis is recommended for relief of immediate symptoms, or a boost in dosage, and it can also be useful for sleep issues. The Cannabis Health Index CHI is an evidence-based scoring system for cannabis in general, not just CBD effects and its effectiveness on various health issues based on currently available research data.
Using this rubric and based on twenty-one studies, cannabis rated in the possible-to-probable range of efficacy for treatment of depression. Research in called for clinical trials to look into the effectiveness of cannabinoids for bipolar disorder manic depression. It also works on the GABA-glutamate system and the hypothalamic-pituitary-adrenal axis.
Its main role is restoring balance through inhibition when levels are too high and enhancement when they are too low. This is the most likely reason phytocannabinoids in general and CBD specifically are able to regulate depression and anxiety. The scientific inquiry into cannabis over the past several decades has confirmed that it is an effective and safe analgesic for many kinds of pain. Of all the reasons that people use CBD today, pain is the most common. The same can be said of cannabis in general.
In the United States, over seventy million people suffer from chronic pain, which is defined as experiencing over one hundred days per year of pain. Physicians differentiate between neuropathic usually chronic and nociceptive pains usually time-limited , and cannabis works on most neuropathic and many nociceptive types of pain. A number of studies have demonstrated that the endocannabinoid system is both centrally and peripherally involved in the processing of pain signals.
Cannabinoids can be used along with opioid medications, and a number of studies have demonstrated that they can reduce the amount of opioids needed, lessen the buildup of tolerance, and reduce the severity of withdrawal. It is suggested that patients work with a health care practitioner experienced in recommending CBD oil or medicinal cannabis so that dosage and delivery methods can be developed and fine-tuned on an individual basis.
Oral CBD products with a ratio of Most discussions of treating pain with CBD suggest that finding the right dosage is critical. Always start with the micro dose to test sensitivity and go up as needed within the dosing range by body weight until symptoms subside. If CBD-dominant products alone are not enough to treat a particular case, products with a higher ratio of THC are sometimes recommended to better manage pain.
For day use, more stimulating, sativa varieties with higher concentrations of myrcene could be added to the formula. In general, for pain, and especially for evening and nighttime, indica strains are favored for their relaxing, sedative effect. A person without experience with THC should use caution and titrate slowly up to higher doses.
Research as well as patient feedback have indicated that, in general, a ratio of 4: THC is the most effective for both neuropathic and inflammatory pain. Each individual is different, however—for some, a 1: Chemotypes high in beta-caryophyllene, myrcene, and linalool provide additional pain relief and increase the effectiveness of other cannabinoids for analgesia. For relief of immediate symptoms, as in a flare-up of pain, vaporizing or smoking work well. The medication effect is immediate and lasts one to three hours, whereas most ingested products take thirty to sixty minutes before taking effect faster on an empty stomach and last six to eight hours.
Sublingual sprays or tinctures taken as liquid drops also take effect quickly and last longer than inhaled products. When pain is localized, topical products can be applied. Topicals affect the cells near application and through several layers of tissue but do not cross the blood-brain barrier and are, therefore, not psychoactive. The skin has the highest amount and concentration of CB2 receptors in the body. Considering all of the studies together, which number over forty for various types of pain , CBD and cannabis are shown to have a rating of likely probable efficacy.
It is one of the best-substantiated medical uses of cannabinoids. Sativex, a cannabis plant—derived oromucosal spray containing equal proportions of THC and CBD, has been approved in a number of countries for use to treat specific types of pain. Numerous randomized clinical trials have demonstrated the safety and efficacy of Sativex for treatment of central and peripheral neuropathic pain, rheumatoid arthritis, and cancer pain.
A study showed that CBD and CBC stimulated descending pain-blocking pathways in the nervous system and caused analgesia by interacting with several target proteins involved in nociceptive control. Sleep Disorders Insomnia, Sleep Apnea Cannabis and sleep have a complex relationship that is only beginning to be understood by science. In general, for most people, indica strains are more relaxing and effective for sleep disorders, whereas sativa strains are more stimulating and tend to keep people awake.
Several studies conducted between and demonstrated the variable effect of different cannabinoids on sleep. Another study found CBD to be wake-inducing for most subjects, though some reported better sleep a few hours after taking it. However, a significant number of people find THC, even indica strains, will make the mind more active.
For these people, CBD oil can benefit them and tends to work well, providing the relaxation and calm for the mental as well as the physical body. For these people, CBD taken at nighttime as part of a bedtime regime produces a restful sleep, not the alertness produced in the daytime.
This bidirectional effect of CBD is the result of balancing the endocannabinoid system. In relation to sleep apnea, a animal study observed the ability of THC to restore respiratory stability by modulating serotonin signaling and reducing spontaneous sleep-disordered breathing.
It is suggested that patients work with a health care practitioner experienced in recommending CBD or medicinal cannabis so that dosage and delivery methods can be developed and fine-tuned on an individual basis.
As mentioned previously, while CBD-dominant products help some people sleep, in others it promotes wakefulness. These tend to be high in myrcene and linalool, a terpene shared with lavender and known to be effective for relaxation.
Cannabis combinations with ratios of 1: THC can be used when patients want to reduce psychoactivity. Oral consumption is recommended as it usually lasts the whole night. The micro to standard dose is usually recommended to treat insomnia and sleep apnea. When relaxing indica strains are used with higher THC levels, a dose of 5—10 mg is usually sufficient. Other people find they need larger doses, such as 15—40 mg.
CBD taken as a tincture or edible will aid in a restful six to seven hours of sleep. This type of disorder varies widely from one patient to the next. Often, one needs to perform some experimental research and try strains of different CBD: For immediate medicinal effects, vaporizing or smoking work well.
This can be helpful for either initial sleep onset or for wakefulness in the middle of a rest period but only lasts one to three hours. The medication effect is immediate, whereas most ingested products take thirty to sixty minutes before taking effect faster on an empty stomach and last six to eight hours.
Vaporizers that use a cartridge filled with the CO2 concentrate are convenient and highly effective, and these are available in various ratios of CBD to THC.
Using this rubric, the use of cannabis-based products for treating insomnia has a rating of likely probable efficacy based on the four studies available at press time 3. A study with the pharmaceutical 1: THC spray showed good results in helping patients with chronic pain sleep better. Four patients in a case series treated with CBD in had prompt and substantial reduction in the frequency of RBD-related events without side effects.
The Dana Forum on Brain Science Trends in Pharmacological Science 36, no. Ashton and Paul F. Van Den Eeden, G. Van Bockstaele New York: Springer, , — Ameritox, , www.
Radulovacki, and David W. Leonard Leinow has three decades of experience growing and studying medical cannabis and brings a unique spiritual perspective to his work. In , he formed Synergy Wellness, a not-for-profit medical cannabis collective in California.
Synergy Wellness has over 3, members in its collective and is an artisan organization making hand-crafted organic and natural whole plant-based products. They are specialists in CBD cannabidiol , the non-psychoactive portion of cannabis, and are pioneers in this aspect of the industry.
The ECS consists of two major types of endogenous G protein-coupled cannabinoid receptors CB1 and CB2 located in the mammalian brain and throughout the central and peripheral nervous systems, including tissues associated with the immune system.
CB1 and CB2 receptors can also co-exist in a variety of concentrations in the same locations. Manipulations of endocannabinoid degradative enzymes, CB1 and CB2 receptors, and their endogenous ligands have shown promise in modulating numerous processes associated with neurodegenerative diseases, cancer, epilepsy, and traumatic brain injury [ Table 1 ].
In addition, the ECS is known to influence neuroplasticity, apoptosis, excitotoxicity, neuroinflammation, and cerebrovascular breakdown associated with stroke and trauma. Phytocannabinoid compounds and extracts can come from both hemp and marijuana subspecies, including CBD. CB1 receptors have the highest densities on the outflow nuclei of the basal ganglia, substantia nigra pars reticulata SNr , and the internal and external segments of the globus pallidus a portion of the brain that regulates voluntary movement.
Very few CB1 receptors are found in the brainstem. These locations suggest CB1 receptor involvement in the modulation of memory, emotion, pain, and movement. In patient studies with chronic pain and neuropathic pain, the use of marijuana or cannabinoid extracts produced positive and improved symptoms. Activation of neuronal CB1 receptors results in inhibition of adenylyl cyclase and decreased neurotransmitter release through blockade of voltage-operated calcium channels. These effects have led to the study of phytocannabinoids for the treatment of epilepsy.
Several pharmaceutical companies are attempting to develop synthetic high-affinity CB1 antagonists and inverse agonists as therapeutic drugs for diabetes, metabolic syndrome, and drug dependence.
Like CB1 receptors, endocannabinoid stimulation inhibits neurotransmission of CB2 receptors. A study of cultured microglial cells showed c-interferon and granulocyte macrophage-colony stimulating factor GM-CSF , known as inflammatory response activators of microglial cell, were accompanied by significant CB2 receptor upregulation. This increased expression was concomitant with the formation of amyloid-beta plaques, suggesting a potential utility for CB2 PET tracers as a diagnostic modality for detecting the onset of neuroinflammation.
Specific cellular targets include neurons, endothelial cells, oligodendrocytes and microglial cells [ 12 , 78 , 92 , ]. Molecular targets of CBD, including cannabinoid and noncannabinoid receptors, enzymes, transporters, and cellular uptake proteins, help to explain CBD's low-binding affinity to both CB1 and CB2 cannabinoid receptors. CBD appears to stimulate synaptic plasticity and facilitates neurogenesis that may explain its positive effects on attenuating psychotic, anxiety, and depressive behaviors.
The mechanisms underlying these effects involve multiple cellular targets to elevate brain-derived neurotropic factor BDNF levels, reduce microglia activation, and decrease levels of proinflammatory mediators. Ingested and absorbed CBD is rapidly distributed, and due to its lipophilic nature can easily pass the blood—brain barrier.
The terminal half-life of CBD is about 9 h and is preferentially excreted in the urine as its free and glucuronide form. Research on the ECS is fervently ongoing with wide-ranging discoveries. The roles of endogenous cannabinoid, phytocannabinoids, and synthetic pharmacological agents acting on the various elements of the ECS have a potential to affect a wide range of pathologies, including food intake disorders, chronic pain, emesis, insomnia, glaucoma, gliomas, involuntary motor disorders, stroke, and psychiatric conditions such as depression, autism, and schizophrenia.
CBD research in animal models and humans has shown numerous therapeutic properties for brain function and protection, both by its effect on the ECS directly and by influencing endogenous cannabinoids. Broadly, CBD has demonstrated anxiolytic, antidepressant, neuroprotective antiinflammatory, and immunomodulatory benefits. CBD decreases the production of inflammatory cytokines, influences microglial cells to return to a ramified state, preserves cerebral circulation during ischemic events, and reduces vascular changes and neuroinflammation.
CBD increases brain adenosine levels by reducing adenosine reuptake. Increased adenosine is associated with neuroprotection and decreased inflammation after brain trauma. These effects have been ascribed to inhibition of glutamate transmission, reduction of calcium influx, reduced microglial activation, and subsequent inhibition of noxious cascades, such as tumor necrosis factor-alpha generation and oxidative stress.
This can contribute to the pharmacological action to reduce nausea. Mechanisms include modulation of excitatory glutamatergic transmissions and synaptic plasticity, modulation of immune responses, the release of antiinflammatory mediators, modulation of excitability of N -methyl-D-aspartate receptors and its effect on gap junctions, calcium, and antioxidants.
Neurodegenerative diseases include a large group of conditions associated with progressive neuronal loss leading to a variety of clinical manifestations. Histomorphological changes can include gliosis and proliferation of microglia along with aggregates of misfolded or aberrant proteins. In addition, a wide range of non-ECS receptors can be influenced by both endogenous and phytocannabinoids. AD is characterized by enhanced beta-amyloid peptide deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits.
Cannabinoids are neuroprotective against excitotoxicity in vitro and in patients with acute brain damage. In human AD patients, cellular studies of senile plaques have shown expression of cannabinoid receptors CB1 and CB2, together with markers of microglial activation.
Control CB1-positive neurons, however, are in greater numbers compared to AD areas of microglial activation. AD brains also have markedly decreased G-protein receptor coupling and CB1 receptor protein expression. Activated microglia cluster at senile plaques is generally believed to be responsible for the ongoing inflammatory process in the disease. In addition, AD-induced microglial activation and loss of neurons was inhibited. AD-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor release, is blunted by cannabinoid compounds.
CBD is effective in an experimental model of Parkinsonism 6-hydroxydopamine-lesioned rats by acting through antioxidant mechanisms independently of cannabinoid receptors. In rats lesioned with 3-nitropropionic acid, a toxin inhibitor of the mitochondrial citric acid cycle resulting in a progressive locomotor deterioration resembling that of HD patients, CBD reduces rat striatal atrophy in a manner independent of the activation of cannabinoid adenosine A2A receptors. Activation of PPAR, along with CB1 and CB2, mediates numerous analgesic, neuroprotective, neuronal function modulation, antiinflammatory, metabolic, antitumor, gastrointestinal, and cardiovascular effects, both in and outside the ECS.
The serotonin receptors have been implicated in the therapeutic effects of CBD. In a rat model, CBD was observed to stimulate hippocampal neurogenesis. Neuroprotective effects of CBD in hypoxic—ischemic brain damage model involve adenosine A2 receptors. CBD activation of adenosine receptors can enhance adenosine signaling to mediate antiinflammatory and immunosuppressive effects. MS is an autoimmune disease that promotes demyelination of neurons and subsequent aberrant neuronal firing that contributes to spasticity and neuropathic pain.
The pathologic changes of MS include neuroinflammation, excitotoxicity, demyelination, and neurodegeneration. These pathological features share similarities with other neurodegenerative conditions, including AD and cerebral ischemia. The combination of antiinflammatory, oligoprotective, and neuroprotective compounds that target the ECS may offer symptomatic and therapeutic treatment of MS.
The use of cannabis-based medicine for the treatment of MS has a long history and its interaction with the ECS shares many of the same pathways of other neurodegenerative conditions. In , the American Academy of Neurology AAN published a review article of 34 studies investigating the use of medical marijuana as extracts, whole plants and synthetic phytocannabinoids for possible neurological clinical benefits. They found strong support for symptoms of spasticity and spasticity-related pain, excluding neuropathic pain in the research using oral cannabis extracts.
They reported inconclusive support for symptoms of urinary dysfunction, tremor, and dyskinesia. This study was subsequently used to form a consensus statement for their society. In the article they concluded their results based on the strength of the reported research [ Table 3 ]. Conclusions from Subcommittee of the American Academy of Neurology AAN systematic review on medical marijuana in neurologic diseases published in [ 66 ]. MS animal models using autoimmune encephalomyelitis EAE have been used that demonstrate demyelination, neuroinflammation, and neurological dysfunction associated with infiltration of immune cells into the CNS consistent with the human disease.
Upregulation of endocannabinoid tone protects neurons from excitotoxicity in parallel with a therapeutic effect in a mouse model of MS. In a week trial with a tolerated dose of 9-THC, subjects had reduced urinary incontinence, and a month follow-up demonstrated an antispasticity effect.
CBD acts specifically to enhance adenosine signaling which increases extracellular adenosine, not AG Neuroprotective effects of CBD in hypoxic—ischemic brain damage also involve adenosine A2 receptors.
Specifically, CBD diminishes inflammation in acute models of injury and in a viral model of MS through adenosine A2 receptors. OPCs are highly vulnerable to inflammation and oxidative stress. Inflammation contributes to demyelinating diseases such as MS. Synthetic cannabinoids studies have shown they can protect OPCs possibly by controlling endoplasmic reticulum ER stress response that modulates the response to inflammatory stimuli. It is an oral-mucosal spray containing a 1: The ability to modify pain may be attributed to a CB receptor-mediated regulation of supraspinal GABAergic and glutamatergic neurons.
The results of these studies were cited in the AAN review. A meta-analysis in reported that CB receptor-based medications were superior to placebo in the treatment of MS-related neuropathic pain. Overall, the analgesic response to cannabinoids was generally retained over time, at least for the 6—10 weeks follow-up period. CBD is recognized as a nonpsychoactive phytocannabinoid. Both human observational and animal studies, however, have demonstrated a broad range of therapeutic effects for several neuropsychiatric disorders.
CBD has positive effects on attenuating psychotic, anxiety, and depressive-like behaviors. The mechanisms appear to be related to the CBD's benefit to provide enhanced neuroprotection and inhibition of excessive neuroinflammatory responses in neurodegenerative diseases and conditions. Common features involving neuroprotective mechanisms influenced by CBD—oxidative stress, immune mediators, and neurotrophic factors—are also important in conditions such as posttraumatic stress disorder PTSD , postconcussion syndrome, depression, and anxiety.
Many studies confirm that the function of the ECS is markedly increased in response to pathogenic events like trauma. This fact, as well as numerous studies on experimental models of brain trauma, supports the role of cannabinoids and their interactions with CB1 and CB2 as part of the brain's compensatory and repair mechanisms following injury.
Animal studies indicate that posthead injury administration of exogenous CBD reduces short-term brain damage by improving brain metabolic activity, reducing cerebral hemodynamic impairment, and decreasing brain edema and seizures. These benefits are believed to be due to CBD's ability to increase anandamide. Treatment with CBD may also decrease the intensity and impact of symptoms commonly associated with PTSD, including chronic anxiety in stressful environments.
In human studies, subjects introduced to fearful contexts exhibited decreased posttest anxiety when treated with CBD. In rodent models, CBD effectively blocked the formation of fearful memories. Rat trials also show CBD's potential in fear memory extinction, demonstrated through a significant decrease in freezing time when re-exposed to an anxiety-inducing situation.
Antidepressants, used for the treatment of depression and some anxiety disorders, also possess numerous neuroprotective properties, such as preventing the formation of amyloid plaques, elevation of BDNF levels, reduction of microglia activation, and decreased levels of proinflammatory mediators. In rat models of neurobehavioral disorders, CBD demonstrated attenuation of acute autonomic responses evoked by stress, inducing anxiolytic and antidepressive effects by activating 5HT1A receptors in a similar manner as the pharmaceutical buspirone that is approved for relieving anxiety and depression in humans.
A double-blind, randomized clinical trial with CBD reported a significant clinical improvement similar to the antipsychotic amisulpride, but with less side effects. Human imaging studies have demonstrated CBD affects brain areas involved in the neurobiology of psychiatric disorders.
A study has showed that a single dose of CBD, administered orally in healthy volunteers, alters the resting activity in limbic and paralimbic brain areas while decreasing subjective anxiety associated with the scanning procedure.
In healthy volunteers treated with CBD and submitted to a presentation of fearful faces, there was a decrease of the amygdala and anterior and posterior cingulate cortex activities and a disruption in the amygdala—anterior cingulated cortex connectivity.
Interestingly, THC, administered prior to a traumatic insult in human case studies and animal models has had measurable neuroprotective effects.
In general, conditions associated with chronic stress appear to be positively responsive to phytocannabinoids. Studies in rat models reported that cannabinoids prevented the effects of acute stress on learning and memory and improved neuroplasticity, behavioral, and neuroendocrine measures of anxiety and depression. Cancer is a disease characterized by uncontrolled division of cells and their ability to spread. Novel anticancer agents are often tested for their ability to induce apoptosis and maintain steady-state cell population.
In the early s, phytocannabinoids were shown to inhibit tumor growth and prolong the life of mice with lung adenocarcinoma. Later studies have demonstrated cannabinoids inhibited tumor cell growth and induced apoptosis by modulating different cell signaling pathways in gliomas, lymphoma, prostate, breast, skin, and pancreatic cancer cells as well.
Glioblastoma multiforme GBM is the most frequent class of malignant primary brain tumors. CBD has also been shown to reduce the growth of different types of tumor xenografts including gliomas. The mechanism of action of CBD is thought to be increased production of ROS in glioma cells, thereby inducing cytotoxicity or apoptosis and autophagy.
CBD also reduces angiogenesis through actions on both tumor and endothelial cells. Median survival was greater than days compared with days in the placebo group.
Reports of cannabis use in the treatment of epilepsy appear as far back as BC. Scientific reports appear in from neurologists using Indian hemp to treat epilepsy with dramatic success. CBD, however, produces antiepileptiform and anticonvulsant effects in both in vitro and in vivo models. More recently in , Cunha et al.
Each patient received — mg daily of CBD or placebo along with antiepileptic drugs for up to 4 months. In the placebo group 1 of 8 responded with fewer seizures. These all suggest that CBD, the nonpsychoactive compound of cannabis, potentially can be helpful for controlling medication refractory seizures. As with most cannabinoid research to date, conducting studies can be difficult due to limited legal access to medical grade marijuana and phytocannabinoid extracts.
Hemp-derived CBD, however, has recently experienced less regulation and as a result research using CBD for refractory epilepsy has experienced a resurgence. CBD's overall effect appears to result in reduction of neuronal hyperactivity in epilepsy. Anandamide affects excitability in neuronal networks by activating the transient receptor potential TRP cation channel. Endogenous cannabinoids appear to affect the initiation, propagation, and spread of seizures. Studies have identified defects in the ECS in some patients with refractory seizure disorders, specifically having low levels of anandamide and reduced numbers of CB1 receptors in CSF and tissue biopsy.
Although this study exclusively looked for effects on seizure incidence, no evidence suggests that the antiseizure effects of CBD are limited to the treatment of this condition. Development of synthetic forms of CBD is also in progress to treat seizure and other disorders responsive to the phytocannabinoid CBD. A comprehensive safety and side effect review of CBD in on both animal and human studies described an excellent safety profile of CBD in humans at a wide variety of doses.
CBD does have interactions with common hepatic drug -metabolizing enzymes, belonging to the cytochrome P family. Therefore, interactions with drug transporters and interactions with drugs must be considered.
In contrast to THC, CBD does not alter heart rate, blood pressure, or body temperature, does not induce catalepsy, nor alter psychomotor or psychological functions. The AAN review of 34 articles on MS using cannabinoids of various forms noted several adverse effects. Reported symptoms included nausea, increased weakness, behavioral or mood changes or both , suicidal ideation or hallucinations, dizziness or vasovagal symptoms or both , fatigue, and feelings of intoxication.
Psychosis, dysphoria, and anxiety were associated with higher concentrations of THC. However, no direct fatalities or overdoses have been attributed to marijuana, even in recreational users of increasingly potent marijuana possibly due to lack of endocannabinoid receptors in the brainstem. Like other cannabinoids, CBD produces bell-shaped dose—response curves and can act by different mechanisms according to its concentration or the simultaneous presence of other cannabinoid-ligands.
Ultimately, prescribing medical marijuana either as a primary treatment or adjunctive therapy will require extreme care and knowledge about the patient's goals and expectations for treatment. States that have allowed medical marijuana have generally required competency trainings and certification prior to prescribing.
There are general screening questions that should be considered before recommending marijuana to a patient. At minimum, these questions should include the following: Although these medications are often cited in human clinical research, their general use is limited based both on side effects and indication constraints. Although federal and state laws are inconsistent about the legality of cannabis production, its increasingly documented health benefits make it once again relevant in medicine.
Current research indicates the phytocannabinoids have a powerful therapeutic potential in a variety of ailments primarily through their interaction with the ECS. CBD is of particular interest due to its wide-ranging capabilities and lack of side effects in a variety of neurological conditions and diseases.
Because of the rapid legalization of medical marijuana by the majority of state legislatures in the U. Because of federal restrictions on human research in the U. This review of the neurological benefits of phytocannabinoids has demonstrated significant benefits for neuroprotection and disease reductions in a wide variety of neurological diseases and conditions in humans.
The Authors report the following conflicts: National Center for Biotechnology Information , U. Journal List Surg Neurol Int v. Published online Apr Author information Article notes Copyright and License information Disclaimer. Received Feb 5; Accepted Feb This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.
This article has been cited by other articles in PMC. Cannabidiol, deltatetrahydrocannabinol, endocannabinoid system, neurological disease, phytocannabinoids. Open in a separate window. Cannabinoid receptors Phytocannabinoid compounds and extracts can come from both hemp and marijuana subspecies, including CBD.
Activation of neuronal CB1 receptors Activation of neuronal CB1 receptors results in inhibition of adenylyl cyclase and decreased neurotransmitter release through blockade of voltage-operated calcium channels.
Cultured microglial dells A study of cultured microglial cells showed c-interferon and granulocyte macrophage-colony stimulating factor GM-CSF , known as inflammatory response activators of microglial cell, were accompanied by significant CB2 receptor upregulation. Research on the endocannabinoid system Research on the ECS is fervently ongoing with wide-ranging discoveries. Neuroprotective benefits of phytocannabinoids CBD research in animal models and humans has shown numerous therapeutic properties for brain function and protection, both by its effect on the ECS directly and by influencing endogenous cannabinoids.
Neurodegenerative diseases Overview Neurodegenerative diseases include a large group of conditions associated with progressive neuronal loss leading to a variety of clinical manifestations. Neuroprotection for AD AD is characterized by enhanced beta-amyloid peptide deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits.
Cannabidiol CBD is effective in an experimental model of Parkinsonism 6-hydroxydopamine-lesioned rats by acting through antioxidant mechanisms independently of cannabinoid receptors. Multiple sclerosis CBD and deltaTHC MS is an autoimmune disease that promotes demyelination of neurons and subsequent aberrant neuronal firing that contributes to spasticity and neuropathic pain.
Use of cannabis-based medicine for neurodegenerative conditions The use of cannabis-based medicine for the treatment of MS has a long history and its interaction with the ECS shares many of the same pathways of other neurodegenerative conditions. American Academy of Neurology statement on medical marijuana In , the American Academy of Neurology AAN published a review article of 34 studies investigating the use of medical marijuana as extracts, whole plants and synthetic phytocannabinoids for possible neurological clinical benefits.
MS animal models utilizing deltaTHC MS animal models using autoimmune encephalomyelitis EAE have been used that demonstrate demyelination, neuroinflammation, and neurological dysfunction associated with infiltration of immune cells into the CNS consistent with the human disease.
Neuropsychiatric and brain trauma Cannabidiol CBD is recognized as a nonpsychoactive phytocannabinoid. Antidepressant and neuroprotective properties Antidepressants, used for the treatment of depression and some anxiety disorders, also possess numerous neuroprotective properties, such as preventing the formation of amyloid plaques, elevation of BDNF levels, reduction of microglia activation, and decreased levels of proinflammatory mediators.
Rat models; efficacy of CBD in neurobehavioral disorders In rat models of neurobehavioral disorders, CBD demonstrated attenuation of acute autonomic responses evoked by stress, inducing anxiolytic and antidepressive effects by activating 5HT1A receptors in a similar manner as the pharmaceutical buspirone that is approved for relieving anxiety and depression in humans.
Human imaging studies correlated with CBD Human imaging studies have demonstrated CBD affects brain areas involved in the neurobiology of psychiatric disorders.
Tetrahydrocannabinol Interestingly, THC, administered prior to a traumatic insult in human case studies and animal models has had measurable neuroprotective effects. Utility for glioblastoma multiforme Glioblastoma multiforme GBM is the most frequent class of malignant primary brain tumors. CBD reduces growth different tumor xenografts CBD has also been shown to reduce the growth of different types of tumor xenografts including gliomas.
Intractable epilepsy Cannabidiol Reports of cannabis use in the treatment of epilepsy appear as far back as BC. CBDs reduce neuronal hyperactivity in epilepsy CBD's overall effect appears to result in reduction of neuronal hyperactivity in epilepsy.
Endogenous cannabinoids Endogenous cannabinoids appear to affect the initiation, propagation, and spread of seizures.
Everything you need to know about CBD oil
These qualities are linked to CBD's ability to act on the brain's receptors for serotonin, a neurotransmitter that regulates mood and social. Antidepressant-like effect induced by Cannabidiol is dependent on brain serotonin levels. Sales AJ(1), Crestani CC(2), Guimarães FS(3), Joca. Neuroprotective effects of CBD in hypoxic–ischemic brain damage model involve adenosine A2 receptors. CBD activation of adenosine.