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cbd oil treatment for als

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What is known exactly from the preclinical models and experimental models with animals? Use of the experimental models has allowed studying the endocannabinoid system in the disease, and as in other diseases, it has been seen that certain elements of the same are altered and that we can modulate these changes for the sake of adjusting a specific treatment.

By way of an explanation, the endocannabinoid system, like other neurotransmitter systems such as the glutamate or the dopamine system, is formed by various receptors in different cells. The main ones are the CB1 receptor (of neurons and which the activation of which produces the psychoactive effects of Δ 9 -THC) and CB2 (characteristic of glial cells and mediator of inflammatory effects). These, in a natural manner, are activated by endogenous molecules in the body (in this case, the so-called endocannabinoids), the most well-known being anandamide and 2AG (2 arachidonoyl glycerol), which are regulated by synthetic enzymes (NAPE-PLD and DAGL) and degradation enzymes (FAAH and MAGL). Cannabinoids that come from the Cannabis sativa plant like the aforementioned Δ 9 -THC or the CBD (cannabidiol) and act on the different elements of the endocannabinoid system, are called Phyto cannabinoids.

In addition, this same CB2 receptor overexpression has been found in a new model of ALS with the mutated protein TDP43. As was the case in the SOD1 model, we obtained the same toxic events resulting from a glial activation with a parallel activation of CB2 receptors in these cells. Pharmacological treatment using another selective synthetic cannabinoid, in this case HU-308, once again obtained a delay of the symptoms of the disease and greater survival of motor neurons. This results in mice that develop the disease later with a greater survival.

Now we know the constitution of the endocannabinoid system, most preclinical studies on this system in ALS have been carried out with models of mutated SOD1. The first pharmacological trials were performed with Δ 9 -THC with the idea of increasing the survival of motor neurons through activation of CB1 receptors that these cells possess. Despite obtaining a certain positive effect, it has been found that the best therapeutic effects found have been mediated by the action of the CB2 receptor. This is due to the fact that over the years the role of glial activation has become increasingly relevant (astrocytes and microglia) not so much as a consequence of the ALS, but as a cause of the same. In addition, in parallel, studies on the endocannabinoid system in this model of mutated SOD1 reflected that there was an increase in levels of CB2. With these two premises, pharmacological trials were carried out with the synthetic cannabinoid AM-1241, selective for the CB2 receptor exclusively. This treatment managed to significantly delay the evolution of the disease correlated with a lower glial activation, i.e. less inflammation. Another way studied with these same positive effects was to block the degradation enzyme MAGL. When this enzyme is blocked, the levels of the endocannabinoid 2AG (2-arachidonoyl glycerol) increase more than normal, which leads to a greater activation mainly of the CB2 receptor, and somewhat lower than the CB1.

Doctor in Biochemistry, Molecular Biology and Biomedicine by the Complutense University of Madrid, he focused his thesis on the study of the endocannabinoid system as a therapeutic target in Amyotrophic Lateral Sclerosis. He is currently about to continue his research work at the Boston Tufts University Medical Center. Winner of the #ZonaAzufre of “Somos Científicos: Sácanos de aquí”.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with motor condition that causes the paralysis of the patient and his/her subsequent death. With ALS being a disease without a cure or effective treatment, cannabinoids are presented as molecules able to delay the symptomatology to improve patients’ quality of life.

ALS was described for the first time in 1869 by the French doctor J.M. Charcot. Today it is considered a rare disease, since its prevalence reflects that there are about 2 people who suffer per every 100,000 inhabitants. The condition tends to be more common in men than in women at a ratio 3 to 1. Most cases are considered sporadic, around 90%, while the remaining 10% are cases of family origin, that is, there is genetic inheritance. From sporadic cases studies have been conducted on environmental factors as possible causes of the disease. Pesticides, heavy metals and even excessive physical activity have been the subject of studies without generating a direct relationship due to not having found significant differences in the populations studied. However, in both cases multiple proteins and genes responsible for triggering the ALS have been identified. In the 1990s the first mutation identified was in the gene of the SOD1 protein, which has led to it being the most studied. It was not until 2006 that TDP43 was also identified as another protein the mutation of which is associated with ALS. In recent years other genes have been added to the list of mutations involved, such as FUS, or more prevalent the C9orf72 gene. It should be noted that depending on which protein is involved, in addition to producing a characteristic symptoms of ALS, it can also reflect symptoms of dementia. In any case, most mutations in these genes generally produce an incorrect protein folding and as a result, functional defects that trigger the death of motor neurons.