Study: CBDA Reduces Neurological Symptoms and Spinal Cord Inflammation in Multiple Sclerosis
- New research found that cannabidiolic acid (CBDA) reduces neurological symptoms and key inflammation markers in an animal model of multiple sclerosis (MS), suggesting therapeutic potential for neuroinflammatory diseases.
- The study showed that cannabinoid acids, including CBDA, decrease inflammatory responses by reducing nitric oxide and interleukin-17A release in microglial cells, which are involved in MS-related inflammation.
- CBDA exhibited a complex effect by lowering several inflammatory markers and improving disease symptoms while simultaneously increasing tumor necrosis factor alpha (TNFα) secretion in both cell cultures and MS-affected mice.
- The compounds crossed the blood-brain barrier, reduced microgliosis, astrogliosis, and CD4+ T cell infiltration in spinal tissues, indicating direct action in the central nervous system with potential immunomodulatory roles needing further investigation.
(Photo credit: EcoLink).
New research published in the journal Molecules found that cannabidiolic acid (CBDA) reduced neurological symptoms and key markers of inflammation in an animal model of multiple sclerosis, adding to growing evidence that compounds derived from marijuana have therapeutic potential for neuroinflammatory diseases.
The study was conducted by researchers from Ben-Gurion University of the Negev and focused on how cannabinoid acids affect inflammation linked to multiple sclerosis (MS), a disease marked by immune system dysfunction, glial cell activation, and damage to the central nervous system. Current treatments for MS generally work by altering immune activity in an effort to slow the disease’s progression.
Researchers examined how cannabinoid acids influenced inflammatory responses in several experimental models. In lab testing, exposing BV2 microglia to these compounds reduced lipopolysaccharide-induced expression of inducible nitric oxide synthase by 40% to 90%. The treatment also lowered the release of nitric oxide and interleukin-17A, both of which are associated with inflammatory activity.
Among the compounds tested, CBDA showed a more complex effect. Although it reduced several inflammatory markers and was linked to lower neurological scores in mice with MS-like symptoms, it also increased tumor necrosis factor alpha (TNFα) secretion. In LPS-stimulated BV2 cells, CBDA boosted TNFα release by up to 40%. It also caused a twofold increase in TNFα secretion in splenocytes taken from MS mice compared to untreated controls.
Despite that increase, the researchers found that CBDA significantly improved disease scores, while both cannabinoid acids reduced microgliosis, astrogliosis, and CD4+ T cell infiltration in lumbar spinal cord tissue. The study also found these compounds crossed the blood-brain barrier, allowing them to act directly in the central nervous system.
According to the researchers, the repeated increase in TNFα seen with CBDA across three models points to a distinct immunomodulatory role that could have therapeutic relevance in multiple sclerosis, even as more research is needed to better understand the mechanism and whether the findings translate to humans.