Medical marijuana, marijuana-based therapies for Parkinson’s disease, epilepsy, and other ailments

Researchers from Vanderbilt University Medical Center have developed a novel approach to treat symptoms of Parkinson’s Disease and other neurological disorders.

The team, led by Dr. Anthony S. Vliet, MD, and Professor James P. F. Sperry, MD., have identified an endogenous cannabinoid system that has been understudied for its ability to help treat neurological disorders, including Parkinson’s.

Dr. VLiet said his team has developed a cannabinoid receptor, or CB1 receptor, in a mouse model of Parkinson, which could potentially be used to treat neurological diseases in humans.

He said the system, which has the ability to bind to receptors on the nervous system, can be used as a therapeutic agent, for example to treat a neurological disorder such as Parkinson’s or Alzheimer’s disease.

“The mouse model is a very interesting animal model that is the first model that has shown that the cannabinoid system can be activated to treat diseases in a natural way,” Dr. Sloris said.

“It is also very interesting because this system has a very low toxicity, and in fact, there are some drugs that inhibit it.”

The researchers found that the CB1 cannabinoid receptor was involved in regulating activity of the cannabinoid receptor gene, resulting in decreased signaling through the CB2 receptor, which is a less important gene in Parkinson’s, and a reduction in signaling through CB3, which in Parkinson has been shown to be a major target for the drug treatment.

The researchers also found that activation of the CB3 receptor reduced activity of CB1 receptors, and that CB1 agonists did not inhibit activation of either the CB5 or CB6 receptors.

“There are a number of drugs that we have found that can affect the expression of the gene but do not actually affect its function,” Dr, Slores said.

The CB1-specific receptor is found in many tissues throughout the body, including the brain, muscle, and joints, and it has also been shown in some animal models to modulate cell signaling in other tissues.

Drs.

Sliet and Vliot found that activating CB1 in the mouse model resulted in decreased CB1 signaling, as well as increased CB1 binding to the CB receptors.

A CB1 antagonist decreased CB5 binding to CB1, but this caused CB1 to bind more strongly to CB2 receptors, which were more important in the brain.

Dr Sloros noted that the effects of CB3 agonists on brain signaling are less clear, and the role of CB2 agonists remains unclear.

He believes the CB system is involved in the modulation of brain activity and that its activation can be targeted to treat certain diseases.

He also believes that this mechanism could be used for other diseases, such as chronic pain.

The study was published online in the journal Neuron.