Vitamin D reduced the signs of inflammation and nerve damage in a rat model of progressive multiple sclerosis (MS), a study shows. Low levels of the vitamin have been extensively linked with a higher risk of developing relapsing forms of the disease, but studies of vitamin D supplementation in MS patients have yielded conflicting results. Recent data suggest it may help prevent disease progression in progressive forms of MS, even though more research is needed. The study, “Vitamin D — An Effective Antioxidant in an Animal Model of Progressive Multiple Sclerosis,” was published in Nutrients. Vitamin D deficiency is thought to be a risk factor for neurodegenerative diseases, including MS, an autoimmune condition caused by an inflammatory response that targets parts of the brain and spinal cord. In several studies, however, vitamin D, even at high doses, failed to reduce relapse rates with relapsing-remitting MS, which is marked by relapses when symptoms suddenly worsen and are interspersed with periods of remission when they ease or fade away. But few studies have investigated vitamin D's impact on the progressive forms of the disease, including primary and secondary progressive MS, which feature a steady increase in disability and worsening of symptoms, even when relapses are absent. Progressive MS and vitamin D. Scientists at the University of Graz, Austria tested vitamin D in a rat model that mimics many features of progressive MS, including damage to the cerebral cortex, the outer layer of the brain. At three weeks of age, the animals were treated with an oral vitamin D solution of 400 international units (IU) a week. Control animals received standard rodent food. The rats were then injected with myelin oligodendrocyte glycoprotein (MOG), a protein that triggers an immune attack on the myelin sheath, the protective fatty coating on nerve fibers that's damaged in MS. They were then infused with immune signaling proteins, called cytokines, that let MOG access the brain and cause damage to the cortex, mimicking progressive MS features. Vitamin D-treated rats had less myelin loss in the cortex and significantly reduced activation of microglia, the brain’s resident immune cells, than the untreated ones. Reduced cell death and the improved preservation of cortical nerve cells were also associated with vitamin D. Microscopic imaging of cortex tissue showed consistent results, including the preservation of neurofilaments, proteins that give structure to nerve cells. Blood tests showed elevated levels of neurofilament light chain (NfL), a marker for nerve cell damage, in progressive MS rats over the unaffected control rats. However, the vitamin D-treated animals had significantly lower NfL levels than untreated progressive MS ones, indicating the supplementation limited nerve damage. Markers that indicated remyelination were also increased in the treated animals. "Since NfL rises upon [nerve] damage, we conclude that [vitamin D] supplementation preserved [nerve] cell structures in our animal model, although not fully suppressing the pathology [disease]," the scientists wrote. Similar trends were seen with two markers of oxidative stress, a type of cell damage that further activates the immune system. Vitamin D in progressive MS rats significantly increased their ability to neutralize oxidative stress. “[Vitamin D] seems to have potential as a supplement in progressive MS, which is why much more research on [vitamin D] in progressive MS and associated animal models is required,” the researchers said.