NOTE: Although I will review any claims for cures of the MS virus, this page is my latest, and last, literature review. It’s a waste of time.
For 50 years I have watched the research community pursue directions funded by pharmaceutical interests while millions of people languish.
Why continue animal research that proves repair of myelin is the natural response to damage, when experts ignore the critical importance of movement and intent in the recovery process?
Once again physics research has proven that events at the quantum level are not related to events at the macroscopic (out here) level, but MRI investigations continue.

Zyga Lisa (2017) Probability that the quantum world beys local realism is less than one in a billion, experiment shows. Physical review Letters July 20 2017.
Wenjamin Rosenfeld et al. Event-Ready Bell Test Using Entangled Atoms Simultaneously Closing Detection and Locality Loopholes. Physical Review Letters. DOI: 10.1103/PhysRevLett.119.010402

Jan 9, 2018

Curr Opin Neurol. 2016 Jun;29(3):286-92.
Repair strategies for multiple sclerosis: challenges, achievements and perspectives. Stankoff B1, Jadasz JJ, Hartung HP, Küry P, Zalc B, Lubetzki C.  Sorbonne Universités UPMC Univ Paris 06, UMR_S 1127, ICM-GHU Pitié-Salpêtrière bINSERM U1127 cCNRS UMR7225 dAssistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière and Hôpital Saint-Antoine, Paris, France eDepartment of Neurology, Medical Faculty, Heinrich-Heine-University of Düsseldorf, Düsseldorf, Germany.
Despite major progress in multiple sclerosis (MS) treatment, to date, accumulation of irreversible clinical disability is not sufficiently prevented with immunotherapies. In this context, repair strategies aimed at reducing axonal damage are becoming a very active field of preclinical and clinical research.
Improved understanding of the cellular and molecular mechanisms of myelin repair, together with the emergence of new therapeutic candidates are paving the way for novel therapeutic strategies in MS. In parallel, there is a very active development of imaging methods to assess lesions ongoing remyelination that are crucially needed to evaluate therapeutic efficacy.
The current development of a very dynamic and multidisciplinary research on remyelination should accelerate the development of myelin repair strategies in MS, to prevent disability progression.

Neurodegener Dis Manag. 2015;5(1):49-59.
Remyelination in multiple sclerosis: what do we know and where are we going? Williams A.
Multiple sclerosis (MS) patients today have more hope of a good disease outcome with an ever-increasing choice of immunomodulatory therapies to reduce disease relapses, thought to be caused by inflammation within the CNS, leading to axonal demyelination. However, although there has been much progress in this disease phase, there has been little impact on the progressive phase of MS, when neurodegeneration dominates and patients accumulate disability over years. This failure of prevention of progressive disease has led to a frame-shift in research thinking, focusing on neuroprotective strategies such as promotion of remyelination, to be used alongside immunomodulatory therapies. This review discusses this unmet need in MS, in terms of pathology and current knowledge of remyelination and proremyelinating therapies.

Prog Brain Res. 2009;175:453-64.
Remyelination in multiple sclerosis. Piaton G1, Williams A, Seilhean D, Lubetzki C. UMRS, Inserm 975, CR-Icm, Paris, France.
Remyelination in multiple sclerosis is in most cases insufficient, leading to irreversible disability. Different and nonexclusive factors account for this repair deficit. Local inhibitors of the differentiation of oligodendrocyte progenitor cells (OPCs) might play a role, as well as axonal factors impairing the wrapping process. Alternatively, a defect in the recruitment of OPCs toward the demyelinated area may be involved in lesions with oligodendroglial depopulation. Deciphering the mechanisms underlying myelin repair success or failure should open new avenues for designing strategies aimed at favoring endogenous remyelination.
[NOTE: EM Deciphering the mechanisms for success, sadly, ignores understanding the critical importance of movement and intention.]

Curr Opin Neurol. 2005 Jun;18(3):237-44.
Promoting repair in multiple sclerosis: problems and prospects. Lubetzki C1, Williams A, Stankoff B.
Fédération de Neurologie, Hôpital de la Salpêtrière, Université Pierre et Marie Curie, Paris, France.
Despite recent progress in treating the inflammatory component of multiple sclerosis, current therapies have no clear impact on progression of disability, which closely relates to tissue (myelin and axon) injury. Many scientists now focus their efforts on elucidating the mechanisms that lead to tissue injury, and on developing new strategies for tissue repair. We review recent breakthroughs in this field and discuss their putative applications to therapy.
Several hypotheses have been raised to explain the failure of remyelination, [NOTE: EM except critical importance of movement.] including depletion of remyelinating cells, quiescence of oligodendrocyte precursor cells and axonal inhibitory signals. Success in remyelination therapy may be achieved either by enhancing endogenous repair or by grafting exogenous remyelinating cells. Several neurotrophic factors have been shown to enhance endogenous remyelination, and many immature cells have been shown to induce efficient exogenous remyelination in animal models. Although effective remyelination probably represents the best way to prevent neurodegeneration, several alternative neuroprotective strategies are emerging. Statins, cyclins and immunophilin ligands are orally available immunomodulatory agents that may protect neurones. Other promising possibilities include the modulation of excitotoxicity, nitric oxide synthesis, or cationic channels. [NOTE from EVA – the suggestion that statin drugs may protect neurones [neurons, nerve cells] is contary to proven destruction of nerves by statin/cholesterol drugs … see NOTE TO LINK HERE TO CHOLESTEROL CONTROVERSY]
Despite the increasing number of putative therapeutic targets, no treatment to achieve remyelination or neuroprotection has yielded positive clinical results in humans. Forging a link between basic biology and treatment of patients will require us to overcome several challenges, [EM including challenge of thorough review of litersture especially Bunge et al 1961] including assessment of efficacy of repair, improving tolerance to and delivery of neurotrophic factors, and better defining the indications for and limitations of transplantation.