Alors que la sclérose en plaques demeure aujourd’hui incurable, une équipe de neuroscientifiques de l’Université de Virginie a fait une découverte majeure, qui pourrait changer la vie des malades. Ils ont en effet identifié le récepteur cellulaire qui provoque la réponse auto-immune et la neuroinflammation caractéristiques de la maladie. Il pourrait s’agir d’une nouvelle cible de choix pour la mise au point de nouveaux traitements.

La progression de cette maladie du système nerveux central peut être freinée grâce une transplantation de cellules souches sanguines, avec environ 80 % d'efficacité. Pourtant, ce traitement reste négligé en France. Ses détracteurs pointent la lourdeur du dispositif et son coût. Explications.

A recent study offers the strongest evidence yet of the link between the Epstein-Barr virus and MS. Not everyone is convinced.

Consistent with the incubation studies, the mouse pharmacokinetic study demonstrated that alcohol decreased the maximum concentration and area-under-the-curve of MMF in the plasma and the brain after dosing with DMF. We conclude that alcohol may markedly decrease exposure to the active MMF metabolite in the plasma and brain potentially decreasing the effectiveness of DMF in the treatment of RRMS.

Brainomix will distribute Neuro.MS, Pixyl’s Software as a Service (SaaS) solution for diagnosis and treatment of patients with multiple sclerosis (MS), exclusively in the UK and Ireland, the Nordics and key markets across Eastern Europe

A little under 10 years ago, Leigh Krauss was almost done with her schooling to become a physical therapist. A former guard on the women’s basketball team at Trinity College in Hartford, Conn., she had always been active and healthy. That is, until one day, walking to class, she lost vision in one eye. Krauss was soon diagnosed with multiple sclerosis, a chronic autoimmune disease where nervous system glitches cause a disconnect between the brain and the body.

Everyone knows that the brain is the command center of the body. This organ is part of the central nervous system that works with the spinal cord and the vital organ systems to send signals that provide motor-sensory functions to make the body do everyday movements. The signals from the brain have a casual relationship with the immune system. When environmental factors enter the body, the brain signals the immune system to send inflammatory cytokines to the area where it was affected and begin the body’s healing process. The immune system helps clean up the body’s cellular structure by replacing old, damaged cells with new, healthy cells. However, when the immune system starts to attack specific parts of the body mistakenly, it can damage the healthy cells causing autoimmune diseases to develop in the body.

Results of this comparative effectiveness research study suggest that inflammation also occurs in patients with PPMS, may contribute to long-term disability, and may be associated with a reduced risk of becoming wheelchair dependent by current licensed DMTs.

Merck’s ‘903 and ‘947 patent are both entitled “Cladribine Regimen for Treating Multiple Sclerosis,” which have been used to produce 10 mg cladribine tablets known as Mavenclad, the complaint said. The patents are listed alongside this drug in the FDA’s “Orange Book” of approved drugs.

The progress that has been made in developing new immune-modifying therapies for MS in recent years is fascinating. Nevertheless, all current drugs fail to prevent neurodegeneration. Moreover, not only are the molecular and cellular mechanisms underlying their effects not completely characterized, but the specificity also needs to be improved in order to spare the protective cellular subtypes.

The presence of persistent intrathecal oligoclonal immunoglobulin G (IgG) bands (OCBs) and lesional IgG deposition are seminal features of multiple sclerosis (MS) disease pathology. Despite extensive investigations, the role of antibodies, the products of mature CD19+ B cells, in disease development is still controversial and under significant debate. Recent success of B cell depletion therapies has revealed that CD20+ B cells contribute to MS pathogenesis via both antigen-presentation and T-cell-regulation. However, the limited efficacy of CD20+ B cell depletion therapies for the treatment of progressive MS indicates that additional mechanisms are involved. In this review, we present findings suggesting a potential pathological role for increased intrathecal IgGs, the relation of circulating antibodies to intrathecal IgGs, and the selective elevation of IgG1 and IgG3 subclasses in MS.

None of the currently available disease modifying therapy is 100% effective in halting disease activity; therefore, it is not unexpected that patients may experience breakthrough disease activity while on therapy during their disease courses. If breakthrough disease activity is observed while the patient has been confirmed to be treatment-compliant, and sufficient time has passed to allow for full physiologic effect of disease modifying therapy since initiation, then a switch should be considered. Response to disease modifying therapy is difficult to define given ambiguity of monitoring criteria.

Natalizumab was associated with superior outcomes over time for many patient-reported health and employment outcomes when compared with other DMTs in this large prospective cohort study. These findings may influence treatment selection in clinical practice and future treatment cost-effectiveness analyses.

Multiple sclerosis is a chronic demyelinating disease of the central nervous system. The underlying cause of this disease is not known, but Epstein-Barr virus is thought to be a possible culprit. However, most people infected with this common virus do not develop multiple sclerosis, and it is not feasible to directly demonstrate causation of this disease in humans. Using data from millions of US military recruits monitored over a 20-year period, Bjornevik et al. determined that Epstein-Barr virus infection greatly increased the risk of subsequent multiple sclerosis and that it preceded the development of disease, supporting its potential role in the pathogenesis of multiple sclerosis (see the Perspective by Robinson and Steinman). —YN

The authors highlight that they have confirmed that the antibody response in the treated patients was significantly lower than in the control groups, in some cases virtually absent, and that this is likely at least partially due to the impaired humoral responses seen in these groups. As well as this, the T cell response to the spike protein is significantly muted in fingolimod-treated patients. The correlation analyses helped show that the length of treatment and reduced capacity to respond to the antibody is likely linked.

The findings suggest that the interactions between the host and the microbiota are reciprocal, although more extensive work is required to confirm this. Moreover, evidence indicates that changes in microbiota composition may result in imbalances that could result in disease, with the gut as a potential novel therapeutic avenue. By understanding the biological effects of aberrant gut microbiome composition, it is possible to contemplate current therapeutic options and their efficacy. Ultimately, more research is necessary in this field, but targeting the gut microbiota may lead to the development of novel therapeutic strategies.

Multiple sclerosis is one of the most detrimental progressive diseases that doesn’t have a cure. Even if it were to be caught early, the current treatment can only slow the progression of multiple sclerosis by reducing nerve cell inflammation and damage. Basically, multiple sclerosis is where the protective coating of nerves in the spinal cord and the brain gets damaged and destroyed by the body’s own immune system. So it can lead to symptoms such as vision loss, muscle spasms, and impaired coordination. Unfortunately, the cause of this disease is unknown.

Progress in finding new treatments for neurologic disorders is often slow and incremental, and it rarely yields therapies that inhibit progression of these diseases. Treatment usually focuses on relieving symptoms. An exception to this pattern is treatment for multiple sclerosis (MS). In the late 1980s, researchers began trials on interferon beta-1b, a drug that was shown to modify MS activity. It was approved by the US Food and Drug Administration (FDA) in 1993.

Multiple sclerosis (MS) is an autoimmune disease. With these conditions, your immune system mistakenly attacks healthy cells. In people with MS, the immune system attacks cells in the myelin, the protective sheath that surrounds nerves in the brain and spinal cord. Dr. David Greene Arizona is developing stem cell therapies to treat these disorders and many autoimmune diseases.

New research shows that the Epstein-Barr virus, a common type of herpes virus, triggers multiple sclerosis by priming the immune system to attack the body’s own nervous system.