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Can cannabinoids be a potential therapeutic tool in amyotrophic lateral sclerosis? This is an open access article distributed under the terms of the Creative Commons ALS is complicated condition that can quickly degrade quality of life – learn how cannabinoids like CBD could help slow the progression of this disease.

Can cannabinoids be a potential therapeutic tool in amyotrophic lateral sclerosis?

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.


Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. Over the last years, a growing interest was aimed to discovery new innovative and safer therapeutic approaches in the ALS treatment. In this context, the bioactive compounds of Cannabis sativa have shown antioxidant, anti-inflammatory and neuroprotective effects in preclinical models of central nervous system disease. However, most of the studies proving the ability of cannabinoids in delay disease progression and prolong survival in ALS were performed in animal model, whereas the few clinical trials that investigated cannabinoids-based medicines were focused only on the alleviation of ALS-related symptoms, not on the control of disease progression. The aim of this report was to provide a short but important overview of evidences that are useful to better characterize the efficacy as well as the molecular pathways modulated by cannabinoids.

Keywords: amyotrophic lateral sclerosis, cannabinoids, symptomatic ALS treatment, experimental ALS model, clinical trials, mechanisms of neuroprotection

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. The incidence is about 1–3 cases per 100,000 population per year. In Italy it is estimated that at least 3,500 patients and 1,000 new cases per year (http://www.osservatoriomalattierare.it/sla). ALS is characterized by relentless progression of muscle wasting and weakness until death ensues typically due to respiratory muscle failure. Generally, ALS patients present a number of clinical symptoms, including weakness, spasticity, cachexia, dysarthria and drooling, and pain secondary to immobility, among others (Zarei et al., 2015).

The most abundant forms of ALS are sporadic (90%), but the disease may be also familiar (10%), associated with mutations in the superoxide dismutase-1 gene (SOD-1), that encodes for a key antioxidant enzyme, and also in TAR-DNA binding protein-43 (TDP-43) and FUS (fused in sarcoma) which encode proteins involved in pre-mRNA splicing, transport and stability (Hardiman et al., 2011). Recently, mutation in non-coding hexanucleotide repeat sequence (GGGGCC) in the C9orf72 gene was considered as the most common genetic cause of ALS (Matamala et al., 2016). The exact function of this protein remains undefined; however, it seems to play a major role in cellular trafficking, mainly in neurons (Williams et al., 2013). The C9orf72 mutation was found also in frontotemporal dementia (FTD) patients (Farg et al., 2014). Since 20% of ALS patients develops dementia with a frontotemporal phenotype, this mutation may explain the link between familial FTD and ALS (Farg et al., 2014).

Although the pathogenic mechanisms that underlie ALS are yet unknown, it is believed that ALS could have a multifactorial etiology, where environmental factors can greatly contribute to pathology triggering. Moreover, several mechanisms including mitochondrial dysfunction, protein aggregation, oxidative stress, excessive glutamate activity, inflammation and apoptosis are involved in ALS pathogenesis leading to motor neuron cell death in the brain and spinal cord (Zarei et al., 2015).

To date, the only therapy available for ALS is the glutamate-antagonist riluzole that was able to inhibit the presynaptic release of glutamate, most likely by blockade of voltage-gated sodium channels. However, riluzole has limited therapeutic efficacy and also it is able to moderately prolong patient survival (Miller et al., 2007). Therefore, new innovative and safer therapeutic approaches are urgently needed, at least aimed at delaying the neurodegenerative processes of the ongoing disease.

Over the last years, a growing interest has been focused to cannabinoids, the bioactive compounds of Cannabis sativa, for their antioxidant, anti-inflammatory and anti-excitotoxic effects exhibited in preclinical models of central nervous system disease (Croxford, 2003). Here, we provided an overview of the potential usefulness of cannabinoid agents in the management of ALS.

Overview on Cannabinoids

The Cannabis plant, also known as marijuana, contains over 500 natural compounds and about 70 of these are classified as cannabinoids (Fischedick et al., 2009). The discovery of Δ9 -tetrahydrocannabinol (THC) as the major psychoactive principle in Cannabis, as well as the identification of numerous non-psychoactive cannabinoids such as cannabidiol (CBD), cannabigerol (CBG), cannabinol (CBN), cannabichromene (CBC), Δ9 -tetrahydrocannabivarin ( Δ9 -THCV) and cannabidivarin (CBDV), has led to a significant growth in research aimed at understanding the therapeutic effects of these compounds.

Cannabinoids exert many of their activities by binding cannabinoid (CB) receptors. To date, two types of receptors have been identified to have different tissue distribution and mechanisms of signaling. CB1 receptors are expressed mainly on neurons and glial cells in various parts of the brain, CB2 receptors are found predominantly in the cells of immune system. Both CB1 and CB2 receptors belong to the family of G-protein coupled receptors (GPCRs) that, after cannabinoid agonist binding and signaling, exert an inhibitory effect on adenylate cyclaseactivity, activation of mitogen-activated protein kinase, regulation of calcium and potassium channels, and other signal transduction pathways (Munro et al., 1993). Moreover, there is increasing evidence supporting the existence of additional cannabinoid receptors (no-CB1 and no-CB2) in both central and peripheral system, identified in CB1 and CB2-knockout mice, involving intracellular pathways that play a key role in neuronal physiology. This kind of receptors includes transient receptor potential vanilloid type 1 (TRPV1), G protein-coupled receptor 55 (GPR55), G protein-coupled receptor 18 (GPR18), G protein-coupled receptor 119 (GPR119) and 5-hydroxytryptamine receptor subtype 1A (5-HT1A) (Pertwee et al., 2010). Δ9 -THC, of which is well-known psychotropic effects, is believed to perform the majority of itsactions in the CNS binding CB1 and CB2 receptors. Non-psychotrophic phytocannabinoids exert multiple pharmacological effects via CB1/CB2 receptors as well as no-CB1 and no-CB2 receptors (Pertwee et al., 2010).

Overall, recent studies showed that cannabinoids inhibit the release of pro-inflammatory cytokines and chemokine in neurological preclinical models suppressing in this way the inflammatory response (Velayudhan et al., 2014). They show also a potent action in inhibiting oxidative and nitrosative stress, modulating the expression of inducibile nitric oxide synthase and reducing the production of reactive oxygen species (ROS) (Velayudhan et al., 2014). Moreover, cannabinoids were found to exert anti-glutamatergic action by inhibiting glutamate release and enhancing the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) (Croxford, 2003). Just about all these properties exhibited by these compounds, have prompted researchers to investigate their potential therapeutic effects in ALS, providing interesting results.

Neuroprotective Effects of Cannabinoids in Experimental Model of ALS

Recent in vivo studies support that cannabinoids may be beneficial as neuroprotective agents in ALS. The most commonly used murine model for human ALS is the hSOD (G93A) transgenic mouse, which is genetically engineered to develop clinical symptoms similar to those observed in humans with ALS.

Treatment with Δ9-THC in ALS hSOD(G93A) mice, either before or after signs onset, improves motor impairment and increases survival by 5% probably via its anti-glutamatergic and anti-oxidant activity (Raman et al., 2004). Moreover, it was demonstrated that Δ9 -THC attenuates oxidative stress in ALS hSOD(G93A) mouse spinal cord primary cultures, that were exposed to the oxidant tert-butyl hydroperoxide (TBH) in the presence of Δ9 -THC and SR141716A, the CB1 receptor antagonist, as assessed by lactate dehydrogenase (LDH) and SOD-1 release. Specifically, the antioxidant effect of Δ9 -THC was not CB1-receptor mediated; since the CB1 receptor antagonist SR141716A did not diminish the antioxidant effect (Raman et al., 2004). Δ9 -THC was found also to protect against excitotoxicity produced by kainic acid in primary neuronal cultures, obtained from ALS hSOD(G93A) mouse spinal cord, by activation of CB1 receptor. In this case, the neuroprotective effect was blocked with the CB1 receptor antagonist, SR141716A, indicating a receptor-mediated effect (Raman et al., 2004). Therefore, treatment with cannabinoids may reduce elevated glutamate levels observed during ALS by modulating excitotoxicity events.

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Moreover, treatment with cannabinol (CBN), a non-psychotropic cannabinoid, through its residual affinity to CB1 receptors, is able to delay significantly disease onset in ALS hSOD(G93A) mice subcutaneously implanted with osmotic mini-pumps. However, the molecular mechanisms remain undefined. On the contrary, survival was not affected (Weydt et al., 2005).

Likewise, a significant delay in disease progression was found when CB1/CB2 receptor agonist WIN 55,212-2 was intraperitoneally administered to ALS hSOD(G93A) mice beginning after onset of motor impairment and tremor (at 90 days old), however, survival was not extended (Bilsland et al., 2006). Genetic ablation of the fatty acid amide hydrolase (FAAH) enzyme, which results in raised levels of the endocannabinoid anandamide, prevented the appearance of disease signs in 90-day-old to ALS hSOD(G93A) mice. However, elevation of cannabinoid levels with either WIN55, 212-2 or FAAH ablation had no effect on life span. On the contrary, CB1 deletion had no effects on disease onset in ALS hSOD(G93A) mice, but extend lifespan by 15 days, a 13% increase in survival. Therefore, the beneficial effects exhibited by cannabinoids may be mediated by non-CB1 receptors, but presumably by CB2 ones. Moreover, the neuroprotective effects of cannabinoids were ascribed to a decrease of microglial activation, presynaptic glutamate release and formation of ROS (Bilsland et al., 2006).

Also, it was demonstrated that mRNA, receptor binding and function of CB2, but not CB1, receptors are dramatically and selectively up-regulated in the spinal cords of ALS hSOD(G93A) mice in a temporal pattern paralleling disease progression (Shoemaker et al., 2007). It was found that daily intraperitoneal administration of the selective CB2 agonist, AM-1241, initiated after disease onset in ALS hSOD(G93A) mice, delayed motor impairment and increased survival by 56%. The beneficial effects of cannabinoids could potentially be mediated via CB2 receptor-mediated suppression of microglial/macrophage activation in the spinal cords of symptomatic G93A mice and that CB2 receptors are selectively up-regulated in spinal cords as a compensatory, protective measure (Shoemaker et al., 2007).

Few years ago, the neuroprotective effects of a mixture of two extracts in approximately a 1:1 ratio (2.7 mg of Δ9 -THC and 2.5 mg of CBD) commercially known as Sativex® were investigated by using ALS hSOD(G93A) transgenic mice (Moreno-Martet et al., 2014). Sativex® was found to be effective in delaying ALS progression in the early stages of disease and in animal survival, although the efficacy was decreased during progression of disease. Also, it has been demonstrated that changes occur in endocannabinoid signaling, particularly a marked up-regulation of CB2 receptors in SOD(G93A) transgenic mice together with an increase of N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD) enzyme, which is responsible for the generation of anandamide (N-arachidonoylethanolamine), the ligand of cannabinoid and vanilloid receptors (Moreno-Martet et al., 2014). Therefore, the efficacy of cannabinoids in slowing ALS progression, in extending life expectancy and in reducing the overall gravity of the disease is mainly due to activation of CB2 receptors. More specifically, it was widely demonstrated that drugs activating CB2 receptors, expressed predominantly in immune cells and non-neuronal tissues, successfully improve the symptoms of several inflammatory diseases (Walter and Stella, 2004). However, further studies are necessary to assess the neuroprotective effects of cannabinoids that target CB2 receptors. Molecular mechanisms underlying cannabinoids-driven neuroprotective effects in ALS hSOD(G93A) mice model are illustrated in Figure 1 .

Schematic illustration of the neuroprotective mechanisms of action of cannabinoids into ALS hSOD(G93A) mice.

ALS & CBD Oil: Promising Research on Cannabinoids & Buying Tips

Amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s Disease, is a neurodegenerative disease with no known cause and as of right now, no known cure.

It is a condition in which the nerve cells in the spinal cord, brain and motor cortex degenerate, leaving connections between the body and its muscles damaged, ultimately resulting in muscular atrophy. But, there is some good news: using CBD oil for ALS symptoms may provide sufferers with much-needed relief.

Benefits of Using CBD Oil for Amyotrophic Lateral Sclerosis (ALS)

It seems that ALS strikes randomly, but it primarily affects men between the ages of 40-70. Only 5-10% of cases are deemed to be familial, or hereditary, with the remaining 90-95% of all cases being classified as “sporadic” . Sporadic means the disease occurs without warning or any identifiable cause. It is a cruel, difficult, disease that researchers are working hard to understand, and significant resources are being put toward finding a cure.

At this point in time, the average lifespan for someone suffering from ALS is 3 to 5 years from the onset of symptoms. Unfortunately, the treatment which is currently available works only to slow down the cell deterioration, not stop it. Riluzole is the medication prescribed to slow deterioration, with other medications are typically prescribed in tandem to combat constipation, pain, sleep problems, depression, cramps, and muscle spasms. It is little wonder that people are looking to CBD oil for possible help.

While the research is still very early, cannabinoids may hold promise as a means for slowing the progression of ALS symptoms. However, at this point the research only consists of animal studies, making it yet to be proven as an effective treatment in humans.

If you’re considering trying CBD to help with your ALS, first speak with your doctor —there could be drug interactions or potential health risks you aren’t aware of. You can also reference this chart for a general idea of how taking CBD oil alone, or in conjunction with current ALS medications, could affect you.

Riluzole (slows progression of ALS) Weakness; drowsiness; nausea; decreased lung function; diarrhea; dizziness; muscle stiffness. Cannabinoids like CBD may be able to slow progression of ALS without causing any of these same side effects based on animal studies. Talk to your doctor before using CBD oil with Riluzole as there is an increased risk of liver damage when used together.
Edaravone (slows loss of daily function) Bruising; hives; shortness of breath; gait disturbance; swelling. CBD oil may be able to reduce pain and inflammation and muscle loss enough to maintain daily function without causing the same side effects. There are no known interactions between CBD oil and Edaravone.
Baclofen or Diazepam (for muscle spasticity) Sedation; dizziness; weakness; headache; insomnia; nausea; constipation; increased urination. CBD oil may help reduce muscle spasticity without causing any of these same side effects. Using CBD oil with Baclofen or diazepam may increase central nervous system and respiratory-depressant effects. Do not use together without being monitored by a doctor.
Gabapentin (for pain) Dizziness; unsteadiness; drowsiness; memory loss; lack of coordination; tremors; viral infections; difficulty speaking. CBD oil can relieve pain without causing any of these same side effects. Using CBD oil with Gabapentin may increase central nervous system and respiratory-depressant effects. Do not use together without being monitored by a doctor.
Trihexyphenidyl (to help patients swallow saliva) Blurred vision; dry mouth; drowsiness; dizziness; anxiety; upset stomach. CBD oil may be able to reduce muscle stiffness without causing any of the same side effects. Using CBD oil with Trihexyphenidyl may increase the potential of cognitive and psychomotor impairment; drowsiness; dizziness.
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While CBD oil is not a cure for ALS, it may offer some relief from the disease’s many symptoms.

There are numerous benefits in the use of CBD for ALS sufferers, the most predominant benefits include the slowing of the progression of the disease, pain relief, and the reduction of spasticity.

Effectiveness of Using CBD Oil for ALS

While research and studies are ongoing, it appears that cannabinoids , and CBD specifically, could play a role in treating ALS. CBD might provide symptom relief, but from the presented animal studies, one cannot yet conclude that CBD could treat ALS in humans. Read on for more information…

A study by the Institute of Neurology at University College London examined the effects of cannabinoids on SOD1 mice, which are test mice that have been modified to exhibit some ALS symptoms. The mice were displaying symptoms at the time of testing and were treated with a synthetic cannabinoid. This cannabinoid was shown to “significantly delay disease progression” and produced “significant neuroprotective effects in this model of ALS.”

Another study by the California Pacific Medical Center of San Francisco tested the effects of cannabinoids on excitotoxic and oxidative cell damage, both of which are thought to contribute to the neurodegenerative effects of ALS. Tetrahydrocannabinol (THC) was shown to be an effective treatment in mice if administered either before or after the onset of signs of ALS. If cannabinoids were administered at the onset of tremors, it was found that motor impairment was delayed and survival was prolonged. While this study did not include CBD, it is another example of the way in which these phytocannabinoids from cannabis and hemp plants can offer possible health benefits.

For fully conclusive results, more testing is needed but these results are exciting and promising for extending the quality of life for ALS sufferers.

CBD Oil for Pain

CBD works directly and indirectly with the endocannabinoid system to reduce the way in which pain is experienced in the body. Cannabinoid receptors can be found both within the brain (CB1 receptors) and throughout the body (CB2 receptors). The CB2 receptors are those which are responsible for regulating inflammation and pain. It’s believed that cannabidiol (CBD) works indirectly on CB2 receptors to reduce inflammation throughout the body.

CBD works on non-cannabinoid receptors as well.

Glycine receptors in the central nervous system have a major role in how the body perceives pain. Studies have shown that CBD can increase the effects of these receptors, causing a significant reduction in neuropathic pain.

One study by the University of California looked at the impact of vaporized cannabis on the treatment of neuropathic pain caused by spinal cord injury and disease. The findings showed that cannabis scored similarly to two commonly prescribed pharmaceuticals in terms of analgesic properties. This is significant because CBD and other cannabinoids do not carry the same side effects or risk for addiction as many prescription painkillers.

Finally, a review of CBD studies conducted between 1980 and 2007 found that CBD oil was effective at treating pain with very few side effects. This places CBD oil as a viable alternative to typical pain medications.

CBD Oil for Spasticity

While clinical trials are severely lacking when it comes to CBD and ALS, there is evidence to suggest that positive results can be expected in the treatment of spasticity.

The University of Washington School of Medicine conducted a survey on cannabis use in ALS patients. Of the 131 respondents, 13 said they used cannabis during the previous 12 months. While these numbers are small, the results indicated that cannabinoids may be effective in reducing the symptoms of “appetite loss, depression, pain, spasticity, and drooling.”

The University of Washington Medical Center supports these findings and because cannabis has shown potential for ALS symptoms by providing “muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction,” they have called for more study and research immediately. The researchers even go so far as to say, “Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.”

There may be a lack of research at the moment in relation to spasticity caused by ALS but there are plenty of published studies dealing with other spastic conditions. Numerous published studies point to the benefits of cannabinoids in treating the symptoms of conditions like Parkinson’s Disease and multiple sclerosis . In a 2014 study , for example, Parkinson’s sufferers who had been administered CBD saw a reduction in tremors and spasticity.

How to Use CBD Oil for ALS

The decision to use CBD oil for ALS symptoms is a personal one, and will look different for each person.

Some ALS patients will choose to add CBD oil to their daily routine as a way to keep symptoms under control in a consistent, holistic way, while others will prefer to use CBD oil when their symptoms appear or become problematic.

As an ALS patient, if you find that traditional ALS treatments are not working the way you’d like or you are suffering from the many possible side effects of pharmaceutical medications, CBD oil may be exactly what you’re looking for.

Before you decide how to take CBD oil for ALS, it is essential that you talk to your doctor first. There are risks associated with using CBD oil in conjunction with common ALS medications, and while CBD oil has very few side effects , and their appearance is rare, there is a possibility of fatigue, dry mouth, diarrhea, and liver damage. Talking to your doctor can help determine if CBD oil is the safest and most effective option.

Different CBD Oil Products

There are a few different ways to administer CBD oil. The CBD product that is most effective for you will depend on your preferences and severity of symptoms.

CBD oil inhalants: CBD vape oils and CBD flower are among the most popular ways to take CBD oil. These delivery methods are familiar and show their effects quickly. The CBD bypasses the digestive system and is absorbed into the bloodstream directly through the lungs. These methods are great for sudden pain or spasticity. But, the effects do not last long, meaning it may be necessary to take another dose an hour or so later. It should be kept in mind that vaping and smoking are not always accessible options and it can be difficult to get the dosage right. Typically, the dosage is calculated on a “per inhale” basis, but an inhale can vary widely from person to person.

CBD oil capsules: CBD oil capsules are easy and convenient delivery methods. Most people will be comfortable with capsules as they are another familiar delivery method and will provide a consistent dose. The same can be said for CBD oil edibles, like gummies. Unfortunately, they can also take a while to show effects. These methods have to be digested and processed by the liver so depending on stomach contents and metabolism, they can take up to an hour to work, but effects typically last 4 to 6 hours.

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CBD Oil Drops or Tinctures : A CBD oil tincture or drops do not have to be digested in the same way as an edible or capsule. Taken under the tongue, the CBD is absorbed from there, going to work in about 30 minutes. They allow for maximum dosage control, with the ability to adjust up or down down to a single drop. In both capsules and drops, the effects can last between 2 to 4 hours.

CBD oil topicals: CBD oil topicals are an option best used for targeted pain relief. For muscle cramps, pain, and spasticity, CBD oil topicals can be applied directly to the site for targeted relief. While these methods can take a while to show effects, they will last the longest of all methods.

Again, it’s essential to consult your doctor before you begin using CBD oil. CBD is mostly safe but it can interact with some of your current prescriptions , including antidepressants and antibiotics. There is also a small percentage of the population that may be sensitive to cannabinoids so it is best to have a doctor monitor your efforts.

For a more in-depth breakdown of all the different CBD delivery methods, check out our Beginner’s Guide to CBD Oil .

Dosage of CBD Oil for ALS

Unless told otherwise by your doctor, always begin by following the recommended dosage on the information sheet included with your CBD product. There is no universal dose of CBD oil, and how it impacts you will depend on a variety of factors like the type of CBD product and your metabolism.

At CBD Oil Review, we have analyzed hundreds of products and come up with a standard serving suggestion to get you started, if you need further assistance:

The CBD Oil Review Serving Standard is 25mg of CBD, taken twice daily

If you are not getting results from this amount, we recommend increasing the serving size by 25mg every 3 to 4 weeks until you find relief.

To better understand how much CBD oil to take, check out our dosage tips here . You should also consider speaking to a naturopathic doctor for an ALS treatment plan that’s personalized for your needs.

Best CBD Oil for ALS

The best CBD oil products for ALS will be the ones that work for you.

Delivery methods should be considered carefully when it comes to ALS. Given that difficulty swallowing is one of the primary symptoms associated with the disease, a CBD oil capsule may only be an ideal format in the early stages of the illness. As it progresses, vapes or tinctures may be easier to administer.

When it comes to reaping the possible benefits of CBD oil, quality matters. It is important you buy the best products available. Here are some hints to help you narrow your search:

  • Look for a Certificate of Analysis (COA): Reputable brands are transparent brands. They will test their extractions in an outside lab and post the results in a Certificate of Analysis. This analysis will tell you exactly what is in your product and allow you to verify the CBD and THC content, while also giving you insight to whether the product contains harmful chemicals, pesticides, or heavy metals.
  • Buy Organic: Whenever possible, buy a product that has been sourced from organically grown hemp. This will ensure that your product is free of residues from herbicides and pesticides.
  • Understand The Law: While the 2018 Farm Bill allows for the legal sale of CBD oil extracted from industrial hemp plants with a THC content of 0.3% or below, some states have restrictions around the sale and purchase of CBD oil. Be sure to know the law in your specific state before making any purchase.

While more research is needed to fully understand all the ways CBD oil can be used to treat ALS, the information currently available is promising. If you’d like to use CBD oil to treat ALS symptoms, remember to speak to your doctor. Together the two of you can work out a safe treatment plan.


  1. Sabrina Giacoppo et al. Can cannabinoids be a potential therapeutic tool in amyotrophic lateral sclerosis? – National Center for Biotechnology Information https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5270417/
  2. Lynsey G Bilsland et al. (2006) Increasing cannabinoid levels by pharmacological and genetic manipulation delay disease progression in SOD1 mice – National Library of Medicine https://pubmed.ncbi.nlm.nih.gov/16571781/
  3. Chandrasekaran Raman et al. (2004) Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid – National Library of Medicine https://pubmed.ncbi.nlm.nih.gov/15204022/
  4. Wei Xiong et al. Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors – National Center for Biotechnology Information https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371734/
  5. Barth Wilsey et al. (2016) An Exploratory Human Laboratory Experiment Evaluating Vaporized Cannabis in the Treatment of Neuropathic Pain from Spinal Cord Injury and Disease – National Center for Biotechnology Information https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5007175/
  6. Ethan B Russo (2008) Cannabinoids in the management of difficult to treat pain – National Center for Biotechnology Information https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503660/
  7. Dagmar Amtmann et al. Survey of cannabis use in patients with amyotrophic lateral sclerosis – National Library of Medicine https://pubmed.ncbi.nlm.nih.gov/15055508/
  8. Gregory T Carter et al. (2010) Cannabis and amyotrophic lateral sclerosis: hypothetical and practical applications, and a call for clinical trials – National Library of Medicine https://pubmed.ncbi.nlm.nih.gov/20439484/
  9. Marcos Hortes N Chagas et al. (2014) Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial – National Library of Medicine https://pubmed.ncbi.nlm.nih.gov/25237116/

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