Background: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system and is the leading cause of neurological disability. Currently, the main strategy for MS therapy is the use of disease-modifying therapies (DMTs). If low-efficacy DMTs are ineffective, patients are transferred to high-efficacy DMTs, which possess more severe side effects associated with immunosuppression. Therefore, the search for new add-on therapies for MS that can enhance the effect of low-efficacy DMTs is relevant. Curcumin, being a natural polyphenol, has immunoregulatory properties and a favorable safety profile. In addition, micellar forms of curcumin can increase its bioavailability. We studied the effect of micellar curcumin on clinical and laboratory parameters in patients with MS receiving low-efficacy DMTs (IFN-β). Methods: Sixty patients with MS and a suboptimal response to IFN-β were randomized (1:1) into two groups: the IFN-CUR group, which received add-on therapy with micellar curcumin (containing curcumin and Tween 80 as a solubilizer) for 6 months, and a control group (IFN group), which received IFN-β alone. The 6-month treatment period was followed by a subsequent 6-month follow-up off curcumin treatment (DMTs only). Results: The proportion of patients without relapses in the curcumin add-on group increased significantly after 6 months (from 57% to 90%, p = 0.007), and the risk of exacerbation was significantly lower compared to the control group (HR = 0.2; p = 0.03). The treatment was associated with EDSS score stabilization, a positive effect on depression (p = 0.05), and a reduction in plasma IFN-γ levels (p = 0.02). A decreasing trend in MRI lesion activity and reductions in specific microbiota-related markers, including the Eggerthella lenta-associated marker (i16a), were also observed. In ex vivo cultures, curcumin significantly inhibited IL-6 production in macrophages derived from patients with multiple sclerosis (MS) and healthy donors. Conclusions: Add-on therapy with micellar curcumin may enhance the efficacy of IFN-β, improving clinical outcomes and modulating inflammatory and microbial parameters in MS patients with a suboptimal response to IFN-β treatment.
Kukushkina et al. (Fri,) studied this question.