Researchers from Temple University School of Medicine have found more evidence supporting the use of marijuana-based treatments in Alzheimer’s disease, stroke and multiple sclerosis.
Inflammation is a common factor in the progression of each of these disorders. But previous studies suggest that marijuana can help control inflammation by acting on specific pathways present in immune cells.
In the latest study, Dr. Yuri Persidsky of Temple University and his team studied the role of these pathways, CB2 receptors, using human cell cultures. Published this month in the American Journal of Pathology, they concluded that activating CB2 receptors could reduce brain tissue damage by preventing immune cells from crossing from the blood stream into the brain.
These results indicate that selective CB2 activation in leukocytes decreases key steps in monocyte-BBB [blood-brain barrier] engagement, thus suppressing inflammatory leukocyte responses and preventing neuroinflammation.
Shilpa Buch, Ph.D, a professor at the Nebraska Medical Center’s Department of Pharmacology and Experimental Neuroscience, noted the importance of the new findings in an accompanying commentary.
None of the previous studies have addressed anti-inflammatory effects of CB2 activation in monocytes in such a comprehensive fashion.
According to Dr. Buch, the migration of immune cells called monocytes plays a critical role in a wide variety of inflammatory diseases.
The development and maintenance of chronic inflammation appear to be underlying causes of numerous human diseases such as atherosclerosis, obesity, diabetes, arthritis, chronic hepatitis, bone disorders, and neurodegeneration (including Alzheimer’s disease, multiple sclerosis and chronic infections of the central nervous system like HIV-1). In all of these diseases, tissue infiltration by monocytes differentiating into macrophages plays a critical role.
Some studies suggest that stimulating CB1 pathways – which are found mostly in the brain and are responsible for the marijuana high – may also have anti-inflammatory potential.
But as Dr. Buch notes, treatments “devoid of the psychoactive effects of CB1 activation” are preferred by doctors.
And while a CB2-specific treatment has yet to be tested in humans, she adds that previous studies have already shown promising results in animal models of atherosclerosis, multiple sclerosis, Alzheimer’s disease, liver and kidney injury and arthritis.
The study was published ahead of print and received funding from the National Institutes of Health and the Intramural Research Program of the NIH-NIAAA