Many treatments already in clinical trials involve drugs that are used in other diseases or medications that have not been designed specifically for multiple sclerosis.
Some researchers think that there could exist also an overlapping between Anti-NMDA receptor encephalitis cases and neuromyelitis optica or acute disseminated encephalomyelitis.
[30] Further oral drugs are still under investigation, the most notable example being laquinimod, which was announced in August 2012 to be the focus of a third phase III trial after mixed results in the previous ones.
[31][32] Early trials of the female sex hormone estriol, led in part by Rhonda Voskuhl, have generated interest in reducing symptoms in women with RRMS.
[36] Such is the case the PEGylated version of interferon-β-1a, that has a longer life than normal interferon and therefore it is being studied if given at less frequent doses has a similar efficacy than the existing product.
[39] Preliminary data have suggested that mycophenolate mofetil, an anti-rejection immunosuppressant medication, might have benefits in people with multiple sclerosis.
However, a systematic review found that the limited evidence available was insufficient to determine the effects of mycophenolate mofetil as an add‐on therapy for interferon beta-1a in people with RRMS.
[40] Monoclonal antibodies, which are biological drugs of the same family as natalizumab, have also raised high levels of interest and research.
[44] The main rationale for polytherapy in MS is that the involved treatments target different mechanisms of the disease and therefore, their use is not necessarily exclusive.
[44] While there have been several clinical trials of combined therapy none has shown positive enough effects to merit the consideration as a viable treatment for MS.[44] Regarding neuroprotective and regenerative treatments such as stem cell therapy, while their research is considered of high importance at the moment they are only a promise of future therapeutic approaches.
[30] Disease-modifying drugs represent possible interventions able to modify the natural course of the disease instead of targeting the symptoms or the recovery from relapses.
Phase III programs consist of studies on large patient groups (300 to 3,000 or more) and are aimed at being the definitive assessment of how effective and safe a test drug will be.
Some possible treatments have been published, such as methylprednisolone pulses[55] or riluzole,[56] and some reduction of spasticity was reported in a pilot Italian study on low dose naltrexone[57] but there is nothing conclusive still.
Respect the etiological research, a special genetic variant named rapidly progressive multiple sclerosis[61] has been described.
[63] Pediatric patients constitute a particularly interesting MS population since the clinical onset of the disease is likely very close to the biological one.
Grey matter lesions were observed in the cerebellum of almost all (93.3%) adolescents with pedMS and significantly outnumbered WML, suggesting that the cerebellar cortex is a main target of MS-related pathology in teens.
[65] Personalized medicine refers to the expected possibility of classifying patients as good or bad responders before starting a therapy.
Given concerns regarding tissue deposition of gadolinium-based contrast agents (GBCAs)[70] and evidence that enhancement of lesions is only seen in patients with new disease activity on noncontrast imaging, research is now being carried out to understand and implement what intravenous contrast agents would be reserved for patients with evidence of new disease activity on non-contrast images.
[71][72] The main measure of evolution of symptoms, specially important as an endpoint in MS trials, is the EDSS (extended disability status score).
In this way, the number of patients in this group was low enough to get the interferon approved by the FDA under the orphan drugs act.
[77] Some reports state that those "types" were artificially made up trying to classify RRMS as a separate disease so that the number of patients was low enough to get the interferon approved by the FDA under the orphan drugs act.
Extensive research on multiple sclerosis is being done on what parts of the world have higher rates of MS compared to other regions.
It increases towards the north and south showing that the highest MS rate is at a latitude of around 60 degrees, which are the countries Orkney, Shetland Islands, and Oslo, Norway.
Recent research as of 2019 point to one of the HERV-W viruses (pHEV-W), and specifically one of the proteins of the viral capside that has been found to activate microglia in vitro.
[99] Supporting this study, a monoclonal antibody against the viral capside (Temelimab) has shown good results in trials in phase IIb.
Although genetics is linked to multiple sclerosis, most of the prime perceptivity of the linkage has not been fully characterized as there has not been a big enough sample size available for the research needed.
[104] Cortical atrophy and demyelination along the subpial surface appear early in the disease course but accelerate in progressive stage.