|
|
|
|
~ Parkinson's Disease ~
|
Page Legend
|
|
Preferred Strains
|
|
|
|
Preferred methods to medicate
Raw Kief/Greens
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
- Drops/Oil Dropped under tongue for faster absorption (Soft membrane tissue).
- Sprays, if for internal best applied through nasal sprays for soft tissue. (If Issue is eye's or ear's, apply to correlation)
|
+
+ + + + + Topically for Pain & Direct muscle spasms + + + + ++ |
|
|
Parkinson's Disease
A basic Breakdown, Cannabis & PD Cannabis Aiding in relief of Parkinson's with significant Improvement |
Dr. Patel.
Discussing cannabis treating PD patients testify a reduction of pain and tremors results will very in patients in the amount of relief, from severity, to duration, so on, this video touches on that . |
Parkinson's (PD), Overview:
Parkinson's disease (PD) is a long-term degenerative disorder of the central nervous system that mainly affects the motor system.[1] The symptoms generally come on slowly over time.[1] Early in the disease, the most obvious are shaking, rigidity, slowness of movement, and difficulty with walking.[1] Thinking and behavioral problems may also occur.[2] Dementia becomes common in the advanced stages of the disease.[2] Depression and anxiety are also common occurring in more than a third of people with PD.[2] Other symptoms include sensory, sleep, and emotional problems.[1][2] The main motor symptoms are collectively called "parkinsonism", or a "parkinsonian syndrome".[4][8]
The cause of Parkinson's disease is generally unknown, but believed to involve both genetic and environmental factors.[4] Those with a family member affected are more likely to get the disease themselves.[4] There is also an increased risk in people exposed to certain pesticides and among those who have had prior head injuries,
Parkinson’s a progressive, neurodegenerative disorder of the central nervous system, primarily affecting motor function and intentional muscle movement. One out of every 500 Canadians is affected by Parkinson’s, with roughly 6,600 new cases diagnosed annually. And while the exact cause of Parkinson’s remains unknown, there is hope for better treatment.
Recently, the European Journal of Pain published a study on the effect of cannabis on motor and nonmotor symptoms of Parkinson’s. Conducted by the Rabin Medical Center and Tel Aviv University, the report found that pain symptoms and motor control improved in the 30 minutes following cannabis exposure. The March 2017 issue of Clinical Neuropharmacology reported similar findings, including “significant improvement” in tremors, rigidity, and slowness of movement (bradykinsea), plus quality and duration of sleep and improved pain scores following cannabis treatment.
The cause of Parkinson's disease is generally unknown, but believed to involve both genetic and environmental factors.[4] Those with a family member affected are more likely to get the disease themselves.[4] There is also an increased risk in people exposed to certain pesticides and among those who have had prior head injuries,
Parkinson’s a progressive, neurodegenerative disorder of the central nervous system, primarily affecting motor function and intentional muscle movement. One out of every 500 Canadians is affected by Parkinson’s, with roughly 6,600 new cases diagnosed annually. And while the exact cause of Parkinson’s remains unknown, there is hope for better treatment.
Recently, the European Journal of Pain published a study on the effect of cannabis on motor and nonmotor symptoms of Parkinson’s. Conducted by the Rabin Medical Center and Tel Aviv University, the report found that pain symptoms and motor control improved in the 30 minutes following cannabis exposure. The March 2017 issue of Clinical Neuropharmacology reported similar findings, including “significant improvement” in tremors, rigidity, and slowness of movement (bradykinsea), plus quality and duration of sleep and improved pain scores following cannabis treatment.
The Parkinson’s-dopamine connection
Dopamine is a neurotransmitter, a chemical in the brain responsible for transmitting signals between neurons (nerve cells) and the brain. It also plays a vital role in smooth muscle movement. With Parkinson’s disease, dopamine-producing brain cells begin to deteriorate and eventually shut down. As dopamine levels drop,
the body responds with symptoms that include:
Dopamine is a neurotransmitter, a chemical in the brain responsible for transmitting signals between neurons (nerve cells) and the brain. It also plays a vital role in smooth muscle movement. With Parkinson’s disease, dopamine-producing brain cells begin to deteriorate and eventually shut down. As dopamine levels drop,
the body responds with symptoms that include:
|
Minor symptoms, such as a fingers twitching uncontrollably, are often the first noticeable signs of the disease. But as Parkinson’s progresses, the tell-tale tremors become more prominent and disruptive to daily life. Without healthy, functioning neurotransmitters, such as dopamine, the brain can’t ‘tell’ the body how to move. Patients lose more and more control over their movements as muscles lock, tremor, or spasm violently.
Recent research has found that using cannabis increases dopamine levels in the body, which thereby eases muscle tremors. However, cannabis prescriptions for tremors is nothing new, with cases of cannabinoids being prescribed for parkinsonian symptoms reported as far back as the late 1800s. |
Parkinson Canada welcomed:
Jonathan Zaid, Cannabis & PD Jonathan, the founder of Canadians for Fair Access to Medical Marijuana The Vashon Island Parkinson's Group
Treating Parkinson's with Cannabis - Super Simple Explanation how cannabis benefits PD |
~ How Cannabis Aids ~
The human body naturally creates endocannabinoid compounds that trigger the same receptors as tetrahydrocannabinol, or THC, the cannabis compound that gives you a “high”.
When you use medical cannabis, the cannabinoids within the plant—including but not limited to THC—engage a large network of cell receptors known as the endocannabinoid system. And that’s good news for Parkinson's Patients: the ECS plays an active role in a wide range of bodily functions, including:
When you use medical cannabis, the cannabinoids within the plant—including but not limited to THC—engage a large network of cell receptors known as the endocannabinoid system. And that’s good news for Parkinson's Patients: the ECS plays an active role in a wide range of bodily functions, including:
|
|
Maureen Leehey, MD
Discusses how & why cannabis may help in treatment of PD |
The Brain, Nervous System, Dopamine & PD
Cannabinoids Activating Dopamine production (PD Motor function), Extracellular & Neuro-signal-Regulation
Cannabinoids Activating Dopamine production (PD Motor function), Extracellular & Neuro-signal-Regulation
Dopamine
Researchers have learned that endogenous cannabinoids, internal brain chemicals that activate the system, play a role in tissue protection, immunity and inflammation, among other functions. The cannabinoid system also appears to exert wide influence, modulating the release of dopamine, serotonin and other neurotransmitters.
Cannabinoid type 1 receptors (CB1Rs) are expressed in the basal ganglia where they regulate intracellular levels of cAMP by interacting with Gi/o and other Gs proteins in the direct and indirect pathways, Dopamine levels stimulate a large concentration of the ECS found in the basal ganglia, the part of the brain responsible for voluntary muscle movements. While healthy bodies manufacture adequate levels of dopamine deep in the brain (also near the basal ganglia), people with Parkinson’s have decreased dopamine levels, making it harder for the body to execute intentional muscle movements in PD. adding cannabinoid supplement as mention modulates the release of dopamine facilitating better motor function and more.
Endo-cannabinoid Regulation:
treatment with cannabis lessens motor symptoms and subjective pain in patients with PD and central parkinsonian pain. The improvement in the UPDRS motor score might be explained by the abundance of cannabinoid (CB1) receptors in the globus pallidum and substantia nigra (Sanudo-Pena et al., 1999; Di Marzo et al., 2000)
Another finding with important implications for potential benefits to brain, nervous, & even Immune system, to potentially aid in disorders like Parkinson's, Epilpepsy, MS, Alzheimer's and potentially/hopefully a lot more. The seminal discovery that G-protein-coupled receptors such as CB1 can activate multiple and even opposing signaling cascades (functional selectivity) depending on binding. Different agonists lead to alternate stable receptor conformations that engage selective transduction mechanisms. For CB1 receptors different cannabinoids demonstrated this biased agonism. It is more complicated as even a single cannabinoid ligand can show biased agonism depending on concentration (cannabinoid system can downregulate and upregulate)(Cannabiniods is one of the most dominant/prevalent G protein in the human body, respectively) (Glass, Dragunow, & Faull, 1997; Herkenham et al., 1991; Mailleux & Vanderhaeghen, 1992; Martín et al., 2008). Regulatory proteins ( eg. Anandamide, 2-AG, THC, CBD, CBC, THCA, THCV, etc ) play a role in controlling cannabinoid signaling via CB1 & 2 receptors which plays a role/ regulates most Systems and organs(reviewed in Ref. [37]). There are a number of regulatory proteins that all interact with CB1 to affect signal transduction, as the endocannabinoid system is a regulatory system, creating homeostasis. aiding in the calming of neuro unregulated firing, relieving symptoms of PD, epilepsy, OCD, and more.These findings are in line with a previous study of patients with PD wherein UPDRS and pain scores (PPI and VAS) decreased following treatment with cannabis (Lotan et al., 2014). Quantitative analysis showed a decrease in cold pain threshold in the more affected limb following immediate cannabis exposure
Different ligands of CB1 receptors produced varying endocytic dwell times (the time during which receptors are clustered into clathrin pits together with β-arrestins before endocytosis) that controlled the functional selectivity of this receptor.:CB1 also forms heteromers with CB2 receptors. There is also evidence that CB1 forms heteromers with a number of other G-coupled receptors including D1 and D2, orexin, μ-opioid, and adenosine2A. Little is known about the physiologic role of these G-protein receptor heteromers but there is evidence that they play a role in disease states such as Parkinson's and addictionand with recent studies showing neuroregulation, nerugenesis neuroprotective, anti-inflammatory and neuroplasticity properties Cannabiniod suppliments are sure to aid.
CB1 activation also causes an interaction and transduction via receptor and nonreceptor tyrosine kinases (reviewed in Ref. [20]).The type 1 cannabinoid receptor, CB1, is one of the most abundant G protein coupled receptors (GPCRs) in the human brain, and mediates the psychoactive effects of things such as chocolate or cannabis, . The endocannabinoids (eg, anandamide, naturally produced in the body & in chocolate), phytocannabinoids (eg, Cannabis Δ9-THC, CBD), and synthetic cannabinoids (eg, CP55,940, WIN55,212-2 MADE IN THE LAB, GMO) act as agonists at CB1, evoking various intracellular signaling responses through receptor activation. Typically, these responses include Gαi/o protein-associated phenotypes such as adenylate cyclase inhibition, and extracellular signal-regulated kinase (ERK) phosphorylation. However, unlike most GPCRs, CB1 is understood to couple to different G proteins under different conditions & can travel different directions, adding to the complexity of cannabinoid signaling characterization. understanding of CB1 receptor signaling, focusing on G protein-mediated signaling, & other mediated signaling and on the subsequent regulation of the receptor that follows their activation will better help conclusive studies as to the exact neurostransmitters and mechanisms related to PD,
As well the inoid receptor-interacting proteins 1a and 1b (CRIP1a and CRIP1b) are only known to interact with CB1 receptors. Both CRIP1a and CRIP1b directly interact with the C-terminus of the CB1 receptor but not CB2. Not much is known about the regulation and function of these interacting proteins. Evidence suggests that CRIP1a attenuates CB1 receptor-induced inhibition of Ca2+efflux.37,38 CRIP1a, like CB1, is widely expressed in the brain at high levels. It has been suggested that these regulatory proteins play a critical role in modulating CB1 receptor function in the pathogenesis or neuroadaptive response to Parkinson's, epilepsy, And other Autoimmune, & neuropsychiatric disorders. There are a number of other regulatory proteins that interact with CB1 to affect signal transduction. Some of these are nonspecific G-protein receptors regulators such as G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2. These proteins facilitate desensitization and intracellular trafficking of CB1 receptors . Other regulatory proteins including AP3 and G protein receptor associated sorting protein-1 (GASP1) associate with CB1 and limited number of other G-coupled receptors. These proteins are less promiscuous and associate with only a limited subset of G-coupled receptors. They direct CB1 targeting to lysosomes, a mechanism of downregulation of response.Some of these are nonspecific G-protein receptor regulators such as cannabinoids/G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2 are seen to play a role in symptoms or symptom reduction.
Researchers have learned that endogenous cannabinoids, internal brain chemicals that activate the system, play a role in tissue protection, immunity and inflammation, among other functions. The cannabinoid system also appears to exert wide influence, modulating the release of dopamine, serotonin and other neurotransmitters.
Cannabinoid type 1 receptors (CB1Rs) are expressed in the basal ganglia where they regulate intracellular levels of cAMP by interacting with Gi/o and other Gs proteins in the direct and indirect pathways, Dopamine levels stimulate a large concentration of the ECS found in the basal ganglia, the part of the brain responsible for voluntary muscle movements. While healthy bodies manufacture adequate levels of dopamine deep in the brain (also near the basal ganglia), people with Parkinson’s have decreased dopamine levels, making it harder for the body to execute intentional muscle movements in PD. adding cannabinoid supplement as mention modulates the release of dopamine facilitating better motor function and more.
Endo-cannabinoid Regulation:
treatment with cannabis lessens motor symptoms and subjective pain in patients with PD and central parkinsonian pain. The improvement in the UPDRS motor score might be explained by the abundance of cannabinoid (CB1) receptors in the globus pallidum and substantia nigra (Sanudo-Pena et al., 1999; Di Marzo et al., 2000)
Another finding with important implications for potential benefits to brain, nervous, & even Immune system, to potentially aid in disorders like Parkinson's, Epilpepsy, MS, Alzheimer's and potentially/hopefully a lot more. The seminal discovery that G-protein-coupled receptors such as CB1 can activate multiple and even opposing signaling cascades (functional selectivity) depending on binding. Different agonists lead to alternate stable receptor conformations that engage selective transduction mechanisms. For CB1 receptors different cannabinoids demonstrated this biased agonism. It is more complicated as even a single cannabinoid ligand can show biased agonism depending on concentration (cannabinoid system can downregulate and upregulate)(Cannabiniods is one of the most dominant/prevalent G protein in the human body, respectively) (Glass, Dragunow, & Faull, 1997; Herkenham et al., 1991; Mailleux & Vanderhaeghen, 1992; Martín et al., 2008). Regulatory proteins ( eg. Anandamide, 2-AG, THC, CBD, CBC, THCA, THCV, etc ) play a role in controlling cannabinoid signaling via CB1 & 2 receptors which plays a role/ regulates most Systems and organs(reviewed in Ref. [37]). There are a number of regulatory proteins that all interact with CB1 to affect signal transduction, as the endocannabinoid system is a regulatory system, creating homeostasis. aiding in the calming of neuro unregulated firing, relieving symptoms of PD, epilepsy, OCD, and more.These findings are in line with a previous study of patients with PD wherein UPDRS and pain scores (PPI and VAS) decreased following treatment with cannabis (Lotan et al., 2014). Quantitative analysis showed a decrease in cold pain threshold in the more affected limb following immediate cannabis exposure
Different ligands of CB1 receptors produced varying endocytic dwell times (the time during which receptors are clustered into clathrin pits together with β-arrestins before endocytosis) that controlled the functional selectivity of this receptor.:CB1 also forms heteromers with CB2 receptors. There is also evidence that CB1 forms heteromers with a number of other G-coupled receptors including D1 and D2, orexin, μ-opioid, and adenosine2A. Little is known about the physiologic role of these G-protein receptor heteromers but there is evidence that they play a role in disease states such as Parkinson's and addictionand with recent studies showing neuroregulation, nerugenesis neuroprotective, anti-inflammatory and neuroplasticity properties Cannabiniod suppliments are sure to aid.
CB1 activation also causes an interaction and transduction via receptor and nonreceptor tyrosine kinases (reviewed in Ref. [20]).The type 1 cannabinoid receptor, CB1, is one of the most abundant G protein coupled receptors (GPCRs) in the human brain, and mediates the psychoactive effects of things such as chocolate or cannabis, . The endocannabinoids (eg, anandamide, naturally produced in the body & in chocolate), phytocannabinoids (eg, Cannabis Δ9-THC, CBD), and synthetic cannabinoids (eg, CP55,940, WIN55,212-2 MADE IN THE LAB, GMO) act as agonists at CB1, evoking various intracellular signaling responses through receptor activation. Typically, these responses include Gαi/o protein-associated phenotypes such as adenylate cyclase inhibition, and extracellular signal-regulated kinase (ERK) phosphorylation. However, unlike most GPCRs, CB1 is understood to couple to different G proteins under different conditions & can travel different directions, adding to the complexity of cannabinoid signaling characterization. understanding of CB1 receptor signaling, focusing on G protein-mediated signaling, & other mediated signaling and on the subsequent regulation of the receptor that follows their activation will better help conclusive studies as to the exact neurostransmitters and mechanisms related to PD,
As well the inoid receptor-interacting proteins 1a and 1b (CRIP1a and CRIP1b) are only known to interact with CB1 receptors. Both CRIP1a and CRIP1b directly interact with the C-terminus of the CB1 receptor but not CB2. Not much is known about the regulation and function of these interacting proteins. Evidence suggests that CRIP1a attenuates CB1 receptor-induced inhibition of Ca2+efflux.37,38 CRIP1a, like CB1, is widely expressed in the brain at high levels. It has been suggested that these regulatory proteins play a critical role in modulating CB1 receptor function in the pathogenesis or neuroadaptive response to Parkinson's, epilepsy, And other Autoimmune, & neuropsychiatric disorders. There are a number of other regulatory proteins that interact with CB1 to affect signal transduction. Some of these are nonspecific G-protein receptors regulators such as G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2. These proteins facilitate desensitization and intracellular trafficking of CB1 receptors . Other regulatory proteins including AP3 and G protein receptor associated sorting protein-1 (GASP1) associate with CB1 and limited number of other G-coupled receptors. These proteins are less promiscuous and associate with only a limited subset of G-coupled receptors. They direct CB1 targeting to lysosomes, a mechanism of downregulation of response.Some of these are nonspecific G-protein receptor regulators such as cannabinoids/G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2 are seen to play a role in symptoms or symptom reduction.
Functional multimeric forms of CB1 receptors are common in the brain. Multimeric homodimer forms of CB1 exist throughout the brain and it is thought in some circles that this could be the native state of CB1 receptors.
Anti-Inflammatory Properties
Inflammation is another major issue with PD, the brain and nervous system under inflammation causes a cascade of affects adding to the difficulty/deterioration and symptoms of the ailment.
With the Endo-cannabinoid system acting as a regulator and stabilizer neurons and other wise, and gene transcription modulation properties, although its not fully known to what extent, we do know - Research from 2014 made the groundbreaking discovery that cannabis:
modulates changes to specific molecules called histones. Histones help control gene expression. The research found that THC can cause changes to histones in a way that suppresses inflammation Aiding in the healing and slowing the deterioration process in advanced patients.
Further, studies have shown that:
cannabinoids also downregulate/supress certain inflammatory neurotransmitter proteins called cytokines.
They found that CBD treatment caused levels of pro-inflammatory cytokines to decrease, all the while levels of anti-inflammatory proteins ie. the anti-inflammatory IL-10 are significantly elevated following CBD-treatment, combating existing inflammation.
Cannabis also activates T-regulatory cells, which prevent cells from attacking itself. eg.( Hyper active immune system).
Cannabis promotes cell death in rogue cells. both in the immune & nervous system, is this property very beneficial to aid in healing & halting further secondary damage (like inflammatory secondary damage, which is also inhibited/halted).
The immune imbalance was tentatively corrected by Cannabis as the endocannabinoid system regulates the immune system.
Pain
Pain regulation occurs through ascending and descending pathways at the level of the spinal cord, periaqueductal gray, thalamus and cortex (Baron et al., 2010; Kuner, 2010; Cury et al., 2016). Immediate pain and cold sensation are transmitted to the spinal cord via small myelinated Aδ fibres, whereas delayed pain and heat sensation are transmitted to the spinal cord via small unmyelinated C-fibres (Santiago et al., 2000). Cannabinoid receptors are spread throughout all pain pathways, including axons of the Aδ and C-fibres, more excessively in the former (Bridges et al., 2003; Manzanares et al., 2006). Given these data, there are two possible explanations for our findings: 1) Heat and cold pain are regulated differently following immediate or chronic use of cannabis. There is rapid activation of Aδ receptors, hence the immediate effect on cold sensation causing cold hypoalgesia, and a late effect on C-fibre receptors, which are responsible for heat pain. 2) Different receptors are involved in heat and cold pain: CB1 receptors are responsible for the transduction of cold pain, and TRPV1 receptors are responsible for the transduction of heat pain (Caterina et al., 1997; McKemy et al., 2001). It may be that after chronic use, cannabis causes a TRPV1-mediated release of substance P and calcitonin gene-related protein (CGRP), leading to the excitation of central root ganglion neurons (Tognetto et al., 2001) and, possibly, heat hyperalgesia.
With the Endo-cannabinoid system acting as a regulator and stabilizer neurons and other wise, and gene transcription modulation properties, although its not fully known to what extent, we do know - Research from 2014 made the groundbreaking discovery that cannabis:
modulates changes to specific molecules called histones. Histones help control gene expression. The research found that THC can cause changes to histones in a way that suppresses inflammation Aiding in the healing and slowing the deterioration process in advanced patients.
Further, studies have shown that:
cannabinoids also downregulate/supress certain inflammatory neurotransmitter proteins called cytokines.
They found that CBD treatment caused levels of pro-inflammatory cytokines to decrease, all the while levels of anti-inflammatory proteins ie. the anti-inflammatory IL-10 are significantly elevated following CBD-treatment, combating existing inflammation.
Cannabis also activates T-regulatory cells, which prevent cells from attacking itself. eg.( Hyper active immune system).
Cannabis promotes cell death in rogue cells. both in the immune & nervous system, is this property very beneficial to aid in healing & halting further secondary damage (like inflammatory secondary damage, which is also inhibited/halted).
The immune imbalance was tentatively corrected by Cannabis as the endocannabinoid system regulates the immune system.
Pain
Pain regulation occurs through ascending and descending pathways at the level of the spinal cord, periaqueductal gray, thalamus and cortex (Baron et al., 2010; Kuner, 2010; Cury et al., 2016). Immediate pain and cold sensation are transmitted to the spinal cord via small myelinated Aδ fibres, whereas delayed pain and heat sensation are transmitted to the spinal cord via small unmyelinated C-fibres (Santiago et al., 2000). Cannabinoid receptors are spread throughout all pain pathways, including axons of the Aδ and C-fibres, more excessively in the former (Bridges et al., 2003; Manzanares et al., 2006). Given these data, there are two possible explanations for our findings: 1) Heat and cold pain are regulated differently following immediate or chronic use of cannabis. There is rapid activation of Aδ receptors, hence the immediate effect on cold sensation causing cold hypoalgesia, and a late effect on C-fibre receptors, which are responsible for heat pain. 2) Different receptors are involved in heat and cold pain: CB1 receptors are responsible for the transduction of cold pain, and TRPV1 receptors are responsible for the transduction of heat pain (Caterina et al., 1997; McKemy et al., 2001). It may be that after chronic use, cannabis causes a TRPV1-mediated release of substance P and calcitonin gene-related protein (CGRP), leading to the excitation of central root ganglion neurons (Tognetto et al., 2001) and, possibly, heat hyperalgesia.
Decreased brain cell degeneration
A buildup of neurotoxins that the body cannot eliminate is believed to contribute to Parkinson’s. Studies have found that cannabis can aid cells in the elimination of toxins and other waste products. Ingested cannabinoids support and improve mitochondrial function, which is responsible for cellular respiration, the metabolizing of carbohydrates into energy, and the excretion of waste products. Cannabinoids have also been found to slow neurodegeneration, the leading cause of cell decay and cognitive function impairment among those living with Parkinson’s.
A buildup of neurotoxins that the body cannot eliminate is believed to contribute to Parkinson’s. Studies have found that cannabis can aid cells in the elimination of toxins and other waste products. Ingested cannabinoids support and improve mitochondrial function, which is responsible for cellular respiration, the metabolizing of carbohydrates into energy, and the excretion of waste products. Cannabinoids have also been found to slow neurodegeneration, the leading cause of cell decay and cognitive function impairment among those living with Parkinson’s.
(-) Ion Channels, Nervous system, cannabinoids & PD
Ligand-gated ion channels such as the nicotinic acetylcholine receptor and GABAA receptor are composed of five subunits arranged around a central pore that opens to allow ions to pass through. There are many different subunits available that can come together in a wide variety of combinations to form different subtypes of the ion channel called heteromer. These Ion channels are directly linked to the nervous system and both are regulated by the endo-cannabinoid system to facilitating homeostasis/balance throughout the bodily functions, thus when there is an imbalance in the nervous system, brain or pathways to and from supplementing cannabinoids has shown to start the process of homeostasis throughout.
(Ions Are electrical discharge from "X"/everything/ anything, ions a essential aspect to health at many levels, everything healthy like a shower/waterfalls, to a apple or nature are all (-) Ions, all harmful catagories, are (+) Ions eg. cellphones, power lines, computer etc. Absorb through the pores transported through to the nervous system to be synthesised.)
|
|
|
|
Clinical Studies
~ Study - March, 2014 - Cannabis (Medical Marijuana) Treatment for Motor and Non–Motor Symptoms of Parkinson Disease: An Open-Label Observational Study with significant improvement
~ Study - 10 October 2016 - Effect of medical cannabis on thermal quantitative measurements of pain in patients with Parkinson's disease with significant improvement.
2013 - Study ~ The cannabinoid CB2 receptor-selective phytocannabinoid beta-caryophyllene exerts analgesic effects in mouse models of inflammatory and neuropathic pain
2013 - Study ~ Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma
2007 - Study ~ Cannabinoids and neuroprotection in motor-related disorders.
2006 - Study ~ Role of the Cannabinoid System in Pain Control and Therapeutic Implications for the Management of Acute and Chronic Pain Episodes
2005 - Study ~ Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity in vivo and in vitro: relevance to Parkinson's disease.
~ Study - 10 October 2016 - Effect of medical cannabis on thermal quantitative measurements of pain in patients with Parkinson's disease with significant improvement.
2013 - Study ~ The cannabinoid CB2 receptor-selective phytocannabinoid beta-caryophyllene exerts analgesic effects in mouse models of inflammatory and neuropathic pain
2013 - Study ~ Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma
2007 - Study ~ Cannabinoids and neuroprotection in motor-related disorders.
2006 - Study ~ Role of the Cannabinoid System in Pain Control and Therapeutic Implications for the Management of Acute and Chronic Pain Episodes
2005 - Study ~ Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity in vivo and in vitro: relevance to Parkinson's disease.
Patents
1989 - Antiinflammatory and antimicrobial compounds and compositions
United States Patent 4837228.
US6630507 Autoimmune/CNS Disorders; Cannabiniods as antioxidants & neuroprotectants
US6410588B1 1998-04-14 2002-06-25 anti-inflammatory agents The Mathilda And Terence Kennedy Institute Of Rheumatology Use of cannabinoids as anti-inflammatory agents
United States Patent 4837228.
US6630507 Autoimmune/CNS Disorders; Cannabiniods as antioxidants & neuroprotectants
US6410588B1 1998-04-14 2002-06-25 anti-inflammatory agents The Mathilda And Terence Kennedy Institute Of Rheumatology Use of cannabinoids as anti-inflammatory agents