According to research published in Stem Cell Reports, researchers are making strides in proving that the brain protein fractalkine can slow the progression of multiple sclerosis and other neurodegenerative disorders.
Fractalkine was given to animals with multiple sclerosis that had been induced artificially. They discovered that the medication increased oligodendrocyte development, which is critical for mending damaged myelin-producing cells in the brain and spinal cord in people with MS.
Multiple sclerosis (MS) is an inflammatory illness that affects neurons and impairs the brain’s capacity to connect with the rest of the body by destroying the fatty coating on nerve cells known as myelin. Although there are therapies for multiple sclerosis, which can produce symptoms ranging from moderate impairment to complete paralysis, the disease’s fundamental origins are unknown, and there is presently no way to stop its growth.
Anastassia Voronova, associate professor and Canada Research Chair in Neural Stem Cell Biology, discovered an increase in the development of new oligodendrocytes in the adult brain, which are essential for myelin synthesis but are destroyed by the autoimmune onslaught that causes multiple sclerosis in the embryonic brain. Both patients and clinicians have expressed great hope in stem cell therapy for treating central nervous system (CNS) disorders in recent years.
While we are still in the early stages of developing viable human medicines, there is substantial evidence from prior research to support the use of stem cells. Despite these findings, the dual participation of the neuroinflammatory response complicates stem cell-supported regeneration following CNS damage. This is due to increased inhibitory immune factors at and around the lesion site.
This emphasizes the potential necessity of creating CNS repair treatments capable of altering the inflammatory environment by boosting anti-inflammatory cytokines. This shows that when used as an immune-modulating cellular treatment, mesenchymal stem cells (MSCs) may have beneficial effects in rodent models of spinal cord injury (SCI). We hypothesize that using MSCs to convey the traditional anti-inflammatory cytokine interleukin-13 would improve their therapeutic potential (IL-13).
For example, “if we can replace those missing or damaged oligodendrocytes, then they can generate new myelin, and it is believed that this may limit disease development or possibly heal some of the symptoms,” says Voronova.
In studies with non-transgenic mice, Voronova discovered that fractalkine was safe and effective. Fractalkine has been shown in preclinical testing in mouse models to give nerve protection, but this is the first time it has been studied in animals with the illness.
Voronova and colleagues discovered new oligodendrocytes and active progenitor cells capable of renewing oligodendrocytes in the treated mice’s brains. This remyelination took place in both white and gray tissue. In addition, inflammation, which plays a role in immune-mediated harm, was shown to be decreasing. The treatment’s next steps will include evaluating it in other sick animal models, such as those with neurodegenerative diseases other than MS.
