Grand Challenges


Education: getting Researchers, MSers and Funders to agree on the unmet needs in MS across all phases of the disease.

Multiple Sclerosis Research: Grand Challenges in MS (1): education,

Phases of MS

1. Preventive phase

Epidemiology: Why is the incidence of MS increasing amongst woman? Any causative model of MS has to explain the epidemiology of the disease, including this intriguing observation.

Epidemiology: What are the mechanisms underlying the month of birth effect in MS?

Multiple Sclerosis Research: Grand Challenges in MS (4): month of ...

Experimental medicine: Does vaccinating children at high-risk of developing MS, who are EBV seronegative, with a vaccine to prevent wild-type EBV infection, protect them from developing MS in the future?

Multiple Sclerosis Research: Grand Challenges in MS (5): EBV ...

2. Diagnostic phase

Treatment: Will aggressive induction therapy, with an immune system rebooter, early in the course of the disease (before fixed disability), prevent the development of secondary progressive MS?  This does not need to be all MSers as immune system rebooting will not necessarily work in all subjects. Answering this question will help us to address whether or not MS is a disease driven by the peripheral immune system, i.e. an autoimmune disease, or a degenerative disease that triggers a secondary inflammatory response. Immune system rebooting can be done with bone marrow transplantation or other less intense immunosuppressive drugs (cladribine, cyclophosphamide (RevImmune), alemtuzumab).

Grand Challenges in MS (2): early aggressive therapy....

3. Minimal impairment Phase

Do MSers on long-term natalizumab treatment, i.e. greater than 10 years or more, develop premature ageing of the brain due to the loss of trophic support from bone-marrow-derived stem cells?

4. Moderate impairment Phase

5. Severe impairment Phase

6. Terminal Phase

Grand Challenges in MS (1): education

It appears that the grandest of all challenges in MS research is education; i.e. getting Researchers and MSers to agree on the unmet needs in the field across all stages of the disease. For example, convincing someone with progressive MS of the importance of prevention, making researchers understand the needs of progressive MSers sand importantly getting the reviewers' and funders' of research to understand the why.  

"We have just received the reviewer's comments back from our MRC grant application that involved the repurposing of an anti-viral drug to target EBV in RRMS; I have never had such a dichotomy in opinion in relation to a grant before. The scores wither clustered at the top or bottom end of the scale regarding innovation and international competitiveness. Why? In other words some reviewer's were behind us and wanted the MRC to fund this study, whilst others thought the idea that EBV could be driving MS disease activity to be a worn-out idea that is irrelevant. The problem as I see it is one of poor communication and education; we obviously did not do enough ground work to prepare the field for the hypothesis that underpinned our grant."

"Scientists would hate to admit it but a lot of science, and in particular science funding, is a social science!"

"We are not going to let the rejection get us down. We have picked ourselves up, dusted off our keyboards and have started again. At the heart of our next grant submission will be an international education campaign to make the world realise that we may be onto something when we say EBV is the cause of MS."

"Education, education, education..." Tony Blair, British Prime Minister, 1997.

Grand Challenges in MS (2): early aggressive therapy

In response to yesterday's discussion on whether or not MS is a primary neurodegenerative disease or a primary inflammatory or autoimmune disease. 

"One way of testing this is with very aggressive induction immunotherapy, i.e. an immune system rebooter, early in the course of the disease." 

"Aggressive early treatment that gets rid of autoimmunity will have a short term impact on the disease by suppressing focal MRI activity and relapses, but will have little long-term impact if the disease was neurodegenerative. In other words this treatment strategy should convert relapsing MS into the primary progressive type or more correctly non-relapsing SPMS. As an MSers with early disease and little disability it would take several years for the progressive disease to emerge." 

"This strategy is currently been tested with autologous bone marrow transplantation and alemetuzumab treatment. How long should we wait to declare a victory? 10 years, 15 years, 20 years or longer? The debate on length of follow-up is not trivial, in fact it is very important as it will be used to define a cure.  In other words if an MSer with RRMS is treated with a bone marrow transplantation, or alemtuzumab, and remains free of disease activity (no new MRI lesions, no excess brain atrophy, no relapses and no disease progression) for 20 years or more they would be cured of having MS. If on the other hand they remain free of disease activity for a period of time and then present with progressive disease they clearly will not be cured and MS would be confirmed as being a primary neurodegenerative disease."

"My money is on the former scenario, which is why I classify myself as a promoter of aggressive treatment strategies. The other extreme is therapeutic nihilism, i.e. not treating MS with anti-inflammatory strategies, until you have evidence that anti-inflammatory treatments impact on the long-term prognosis. My problem with therapeutic nihilism is that I don't have the disease and what if the nihilist is wrong? Surely an intelligent MSer armed with the facts, or lack of facts, can make the call? What do you think? I don't want to have regrets."

"Please note that not all MSers will respond to BMT or alemtuzumab; in other words these treatments may or may get rid of autoimmunity. This fraction may not be small, which is why we need large number of MSers in trials and prolonged follow-up."

"Please note all of the above may be wrong and MS could be due to a virus; the virus is what is responsible for causing the damage and if your immune system sees the virus it results in focal inflammation and cause an MRI lesion and possibly a relapse. This is why we have launched The Charcot Project, to test the hypothesis that MS is due to a virus. If you read this blog you will note that we favour EBV and HERVs as being the leading contenders. We may be wrong, we may be right! The only way to find out is to treat MS with targeted anti-virals." 

Finally, I would like to point out the twin that is described in this small series of MSers that underwent a BMT:

Mandalfino P, Rice G, Smith A, Klein JL, Rystedt L, Ebers GC. Bone marrow transplantation in multiple sclerosis. J Neurol. 2000 Sep;247(9):691-5. 

There is strong circumstantial evidence that MS is an autoimmune disease. Nonspecific immunosuppressive therapy has not been successful in altering the natural course of the illness. Bone marrow transplantation has heretofore been a radical therapy used in patients with life-threatening malignancies but has potential as a treatment for human autoimmunity. In MS there have been no controlled studies. We report here four patients with MS undergoing bone marrow transplantation with 6-48 months of follow-up. In three this was carried out for co-existing malignancy and in one as an experimental treatment for MS using the patient's unaffected identical twin as a donor. The limited outcome that can be evaluated in these patients supports further experimentation into this treatment modality in MS patients with poor prognostic indications.

"George Ebers told me that initially this twin did very well; her disability improved and she stabilised without any relapses - she appeared to have burnt out MS. Was she cured? Unfortunately not, about 7 years after her BMT she developed SPMS. This observation would support MS as being a primary neurodegenerative disease. What do you think?"

"This case is not a good example; as she has quite advanced disease and had already acquired a lot of damage she was destined to develop progressive disease. Why should someone with a damaged nervous system be primed for progression? That is another story, possibly another grand challenge."

"I hope this post in not confusing; if it is I will try and simplify the concepts!"


Grand Challenges in MS (3): changing sex ratio

Why is the incidence of MS increasing amongst woman? 

To prove that MS is caused by a single factor or the interaction of several factors it has to explain everything we know about the epidemiology of the disease. 

Epidemiology = the branch of medicine involved with the study of disease in the population; epidemiology deals with the study of the causes, distribution, and control of disease in populations.

One observation that is being noticed across several populations, but not all, is the increasing incidence of MS in woman. Why is this occurring? Some of it may be due to the changing in smoking prevalence amongst woman, which has been increasing relative to males. Another is cultural factors, for example the addition of UV blockers in cosmetics over the last 15 years. Other have suggested the use of oral contraceptive pill (OCP) or change in work environment. However, the change in sex ratio appears to go back to the beginning of the 20th century so it predates the change in work environment associated with World War 2 or the introduction of the OCP in the '60s.


Other posts of interest:

Research: the MS diagnosis just got better in the Netherlands, 26 July 2012; "The increasing incidence amongst woman can be seen with a change in the sex ratio. Why this is occurring is not clear. Some of the increasing incidence can be explained by changes in the rate of smoking amongst woman ...

Research: Sex Ratio with MS increasing in Women, 24 May 2012; METHODS: Since environmental risk factors seem to act early in life, we calculated sex ratios by birth year in 27 074 Canadian patients with multiple sclerosis identified as part of a longitudinal population-based dataset.

Research: More women than men have MS in Sweden, 22 Jun 2012; Methods:Data from the Swedish MS Register and data from the Swedish National Statistics Office were used to estimate sex ratio by year of birth and year of onset. Results:In the analysis of sex ratio by year of birth there were ...

Article of interest (1): change in sex ratio of MS - Multiple Sclerosis ..., 11 Jun 2011; 2006 Nov;5(11):932-6. This study showed that the female to male sex ratio by year of birth has been increasing for at least 50 years and now exceeds 3.2:1 in Canada. "The incidence of MS is increasing; particularly in woman.

Multiple Sclerosis Research: Research:MS in Women
 , 23 May 2012; At the turn of the 1900's Canadian data indicate that the sex ratio of female to males was around is 1 to 1 it is now nearer to 3 to 1. In Iran the ratio is 6:1. MS is increasing in women and staying constant in men. Why is this the ...

Grand Challenges in MS (4): month of birth effect

Why does the month you are born in affect your risk of MS?

I assume you are aware that month of birth is a risk factor for MS. In the Northern hemisphere, if you are born in May you have a higher chance of developing MS compared to people born in November. This month of birth effect is now being attributed to the effect of low vitamin D levels in the womb. The low vitamin D affects how the immature immune system develops. In other words if your mother was pregnant during winter, a time when she was more likely to be vitamin D deficient, your immune system was unable to develop properly and resulted in you being more susceptible to developing an autoimmune disease in later life. In support of the vitamin D hypothesis is the observation that the month of birth effect gets larger the further you are away from the equator, i .e. it is greater in Scotland than it is in England. 

The month of birth effect is not unique to MS and has been observed in type 1 diabetes mellitus, rheumatoid arthritis, ulcerative colitis and systemic lupus erythematosus and schizophrenia. Is schizophrenia an autoimmune disease? This is an interesting question and beyond the scope if this blog, but worthy of some serious thought. The fact that the month of birth effect is found with other diseases implies that it is an important biological phenomenon and worthy of looking into in more detail. 

Therefore the grand challenge is to pin down the molecular and immunological mechanisms of the month of birth effect. This is very important as it will underpin strategies for prevention, for example, vD supplementation in pregnancy, and it will provide potential markers to assess the impact of MS preventative strategies in the future. In other words a successful MS preventative strategy should correct the defect that is associated with the month of birth effect. 

FromWiller et al. Timing of birth and risk of multiple sclerosis: population based study. BMJ. 2005 Jan 15;330(7483):120.

Disanto et al. Month of birth, vitamin D and risk of immune mediated disease: a case control study. BMC Med. 2012 Jul 6;10(1):69. 

BACKGROUND: A season of birth effect in immune-mediated diseases (ID) such as multiple sclerosis and type 1 diabetes has been consistently reported. We aimed to investigate whether season of birth influences the risk of rheumatoid arthritis, Crohn's disease, ulcerative colitis and systemic lupus erythematosus in addition to multiple sclerosis, and to explore the correlation between the risk of ID and predicted ultraviolet B (UVB) light exposure and vitamin D status during gestation.

METHODS: The monthly distribution of births of patients with ID from the UK (n = 115,172) was compared to that of the general population using the Cosinor test. Predicted UVB radiation and vitamin D status in different time windows during pregnancy were calculated for each month of birth and correlated with risk of ID using the Spearman's correlation coefficient.

RESULTS: The distributions of ID births significantly differed from that of the general population (P = 5e-12) with a peak in April (odds ratio = 1.045, 95% confidence interval = 1.024, 1.067, P <0.0001) and a trough in October (odds ratio = 0.945, 95% confidence interval = 0.925, 0.966, P <0.0001). Stratification by disease subtype showed seasonality in all ID but Crohn's disease. The risk of ID was inversely correlated with predicted second trimester UVB exposure (Spearman's rho = -0.49, P = 0.00005) and third trimester vitamin D status (Spearman's rho = -0.44, P = 0.0003).

CONCLUSIONS: The risk of different ID in the UK is significantly influenced by the season of birth, suggesting the presence of a shared seasonal risk factor or factors predisposing to ID. Gestational UVB and vitamin D exposure may be implicated in the aetiology of ID.

Other posts of interest

08 Jun 2012
The place of birth effect (preponderance for more Msers from the North verses the South USA) and month of birth effect (higher in May than November) was not evident. The place of Birth effect had been noticed previously in ...
09 Jul 2012
Month of birth, vitamin D and risk of immune mediated disease: a case control study. BMC Med. 2012;10(1):69. BACKGROUND: A season of birth effect in immune-mediated diseases (ID) such as MS and type 1 diabetes has ...
29 Apr 2011
There is now convincing evidence for an epigenetic component to MS, with maternal parent-of-origin, transgenerational (grandparental) and early life (month of birth) effects, as well as the increasing sex ratio of the disease.
19 Jan 2012
If part of the vitamin D effect is in utero (in the womb), as could be suggested by the month of birth effect. Then the issue of vitamin D levels in MSers at onset etc may be irrelevant. This adds an extra level of complexity. Sunday ...

12 Oct 2011
Vitamin D deficiency in pregnancy is very likely to be an important risk factor and may explain the month of birth effect; i.e. if you mother was pregnant during winter (last 6 months) and you were born in April you are at ...
02 Oct 2011
I suppose Dr Beggs can explain the genetics, latitudinal effect, OCBs, month-of-birth, sex ratio, migration effect, ectopic B cells follicles, gray matter pathology and the EBV-smoking-vD association by CCSVI.
14 Jun 2011
The month of birth and risk of MS are associated, more so in familial cases, implying that there is some interactions between genes and environment that may be related to climate. Such interactions may act during gestation or shortly after birth in individuals born in the countries studied. "The finding ... Vitamin D: effects on immune cell function in MS'e... Vascular aspects of multiple sclerosis: a review · Potential health care cost savings associated with... Research focus...
13 Jul 2011
It appears that the month of birth effect relates to vitamin D's effect on the developing foetus. ReplyDelete. Anonymous Wednesday, July 13, 2011 4:10:00 PM. Re: “What about hope? I still believe that some of the emerging, ...

16 May 2012
... for this effect. The negative associations observed with greater maternal parity and number of siblings are consistent with some other studies. Reasons for these associations may involve various pathways. Month of birth has ...
14 Jun 2012
They tested whether variation in UVR as determined by seasons (short term variation) and solar cycles (long term variation) is related to MS birth month and to survival as measured by lifespan. Methods: Cases were selected ...
28 Jun 2011
Results: At 12 months, the average serum vitamin D concentrations were 83 nmol/liter and 179 nmol/liter in control and treated participants, respectively (P < 0.001). In treated MS'ers, the abnormal immunological responses of ... But what other, less obvious, effects could there be? (Rhetorical question). Tuesday, June 28, 2011 12:15:00 PM. Anonymous said. .... Article of interest (3): month of birth and risk o... Symptomatic liver injury associated with complemen.

Grand Challenges in MS (5): EBV vaccination

As you are aware from reading this blog that EBV is strongly associated with MS and some of us  believe that there is now enough evidence to accept EBV as the cause of MS. One of the reasons for thinking this is that if you are EBV seronegative, i.e. you have never been infected with the virus your chances of getting MS are close to zero. The latest meta-analysis we did showed that when you use two robust assays to assess EBV seronegativity your risk is in fact zero. 

Pakpoor et al. The risk of developing multiple sclerosis in individuals seronegative for Epstein-Barr virus: a meta-analysis. Mult Scler. 2012 Jun 11.

It is also apparent that you have to be infected with EBV before you develop MS; this is the correct sequence of events to prove causation. As you have gathered causation theory is complex and you need to fulfill many criteria; one of these criteria is experimental evidence. In other words if you stop people becoming infected with EBV you should prevent them from developing MS. 

The grand challenge is to develop a vaccine against EBV that prevents wild-type infection and to set-up a study to test this hypothesis, i.e. to take a group of children who are at high risk of developing MS because one or both of their parents have MS, and to vaccinate half of them against EBV and the other half against another virus or with a placebo vaccine, and to then follow them up to see if those vaccinated with the active vaccine have a reduced incidence of MS. The follow-up for this study will have to be for 30-40 years as the average age of onset of MS is 30. To do this experiment we would first need to develop a safe and effective vaccine against EBV. The current vaccines that have been developed are not that effective; they provide some immunity against EBV but not enough to prevent wild-type infection. 

You may find it interesting that when people with leukaemia undergo bone marrow transplantation from a donor of the opposite sex that cells derived from the transplant can be found within the brain several years later. We know these cells are donor derived because in female recipients these cells have a Y or male chromosome. Presumably stem cells from the donor bone marrow are released and migrate into the brain and give rise to new microglia and neurones;  all be the latter in small numbers. 

Grand challenges in MS (6): peripheral stem cell and monocyte migration

Is this important for MS? May be it is! The reason I say this is that bone marrow derived stem cells and monocytes use the same receptor as lymphocytes to cross the blood-brain-barrier, i.e. VLA4. Interestingly and importantly, this is the receptor that is blocked by natalizumab. Natalizumab will therefore block the migration of bone-marrow derived stem cells into the brain and spinal cord. 

Is this dangerous? In the short-term it appears not to be as MSers do very well on natalizumab. But I am worried about the long term effects of natalizumab on bone-marrow derived stem cell and monocyte migration; do our brains and spinal cord lose their ability to repair themselves if they are cut-off from these sources of cells? If they do, natalizumab-treated MSers may be at risk of premature ageing. 

Question: Do MSers on long-term natalizumab treatment, i.e. greater than 10 years or more, develop premature ageing of the brain due to the loss of trophic support from bone-marrow-derived stem cells? 

To answer this question we need long-term monitoring of natalizumab-treated MSers to look for markers of premature ageing, i.e. the premature development of age-related neurodegenerative disorders, for example Alzheimer's, Parkinson's or other age-related neurodegenerative diseases. This adverse event would take decades to emerge; therefore we need to remain vigilant for unexpected biological consequences of reducing trafficking of stem and other cells into the brain and spinal cord.

Why is this a grand challenge? Simply because so many MSers are now on natalizumab and the first MSers treated are getting to the time window when these potential effects would start emerging. And it is something that keeps me awake at night!

Clues to support my anxieties come from the conjoined mice or parabiosis experiments we have posted on before on this blog:

These experiments show that the ageing brain in older mice responded to something from the circulation of younger mice; the factor seemed to be chemical signals that promote cellular migration across the blood brain barrier. It would be interesting to see what would happen in the conjoined twin or parabiosis experiment if the mice were treated simultaneously with mouse natalizumab; i.e. would mouse natalizumab block the brain regenerative effects of youth in the older mice? 

If you are on natalizumab and develop new or unexplained symptoms, that you think may or may not be related to MS, let your MS team know. 

It is clear that B cells play a central role in pathogenesis of MS:

1. MS has not be seen in people who don't make immunoglobulins due to rare genetic disorders (agammaglobulinaemia).

2. Oligoclonal IgG bands are invariably found in the cerebrospinal fluid (CSF) and brain/spinal tissues of MSers. These immunoglobulin bands have been highly selected; in other words whatever is driving their production is getting help from other cells (antigen presenting cells and T cells). This selection process is typically seen with infections or foreign antigens (proteins).

"In my opinion if we can uncover what these bands are reacting with we will uncover or pin down the cause of MS". 

MSers who don't have these oligoclonal bands have a more benign course; this applies to MSers with relapse-onset MS and PPMS.

"In my opinion OCB-negative MSers don't have 'classic MS' and should be given a separate diagnosis or the diagnosis of definitive MS should be delayed; this is particularly important when diagnosing PPMS! This is another reason why lumbar punctures and spinal fluid analysis should be done in all MSers. You only get one chance not to make the diagnosis of MS and that is in the beginning or the diagnostic phase of the disease. Spinal fluid analysis helps you exclude other conditions and tells you if you have OCBs or not." 

3. B-cell follicles, were the B-cells mature and become antibody factories or plasma cells, are found in CNS of MSers. These are ectopic follicles as they are normally found in lymph nodes and the spleen. These follicles appear to be more common in progressive MSers and may result in cortical or gray matter pathology that drives progressive disease.

4. Pathological studies show immunoglobulin deposits in the brains of MSers and complement activation. Complement is one of the molecules that certain classes of immunoglobulins use to damage or kill target cells and organisms. Interestingly in the, now famous, Barnett and Prineus lesion immunoglubluin deposition was seen without the classic T cell infiltrates. Many of us now consider this to be the earliest relapse-causing lesion and based on the observations in these lesions immunoglobulins seem to be is very important inflammatory mediators.

5. B cells are the cells were EBV, the virus that is causally linked to MS, resides.

"Could the B cell be the Trojan horse that takes EBV into the brain and spinal cord? Unfortunately, the evidence on this topic is rather mixed at present, but I suspect the B-cell is the cell that EBV hitches a ride in." 

6. Most if not all highly effective MS DMTs target B cells.

"This is an observation that I made years ago!" 

7. Targeted anti-B cell therapies (anti-CD20 - rituximabocrelizumabofatumumab) are among the most promising emerging MS therapies. There superior efficacy was not expected given the current dogma that MS is T-cell driven disease.

"It is a pity that anti-CD20 therapies do not target plasma cells or plasma blasts; these are the immunoglobulin factory cells and are also part of immunoglobulin pathway. May be the newer anti-CD19 agents that target plasma blasts will be more effective than anti-CD20?"

    The Grand Challenge"Are B cells the pivotal cell in the pathogenesis of MS? How do anti-B cell therapies work in MS? Do anti-B cell therapies work as anti-EBV agents?"

    Other posts of interest:


    07 Mar 2012
    Barnett and Prineas. Ann Neurol. 2004 Apr;55(4):458-68. "I am reposting this for those of you have not had time to read all the posts on this blog." "This study really challenges our understanding of MS; it challenges the dogma ...
    22 Dec 2011
    Ectopic lymphoid follicles (place where antibody producing B cells are generated) are hallmarks of chronic autoimmune inflammatory diseases such as multiple sclerosis (MS), rheumatoid arthritis, Sj√∂gren's syndrome, and ...
    06 Jun 2011
    The B cell that make the antibodies are found in structures called "ectopic lymphoid follicle-like structures" in the coverings of the brain and spinal cord; the covering are called the meninges. These ectopic follicles are not ...
    05 Oct 2011
    The immune system forms and maintains the ectopic B-cell follicles in the brain & spinal cord by producing a cocktail of immune messengers called cytokines. One of these messengers is called lymphotoxin; if you inhibit or ...


    03 Nov 2012
    Background: Recently, the disappearance of oligoclonal bands (OCBs) from the cerebrospinal fluid (CSF) of a few natalizumab-treated MSers has been reported. This is interesting since CSF-restricted OCB are believed to ...
    13 Sep 2012
    BACKGROUND: The use of oligoclonal bands (OCBs) and cerebrospinal fluid (CSF) parameters are established in the diagnosis of MS, but poorly as markers of disease. OBJECTIVE: To investigate the role of OCBs in ...
    19 Nov 2011
    Background: Intrathecal antibody production manifest as oligoclonal bands (OCBs) is a hallmark of multiple sclerosis (MS). Once present, OCBs can be detected in the cerebrospinal fluid that bathes the CNS throughout the ...
    23 Jan 2012
    Correct me if i am wrong, but this means that the OCBs in MS do not necessarily imply a reaction to some pathogen, but could very well be the aftermath of some kind of brain or spinal injury. ReplyDelete. Anonymous Monday ...


    06 Nov 2011
    Current Ocrelizumab Trials that are recruiting subjects. Study 1: A Study of Ocrelizumab in Patients With Primary Progressive Multiple Sclerosis (NCT01194570). Eligibility: Ages Eligible for Study: 18 Years to 55 Years ...
    04 Jun 2011
    Please note that Ocrelizumab is the follow-on compound of Rituximab; both these drugs are monoclonal antibodies that target a protein CD20 that is expressed on B cells. Exactly how these drugs work is not known. However ...
    06 Nov 2011
    At week 24, patients in the initial placebo, 600 mg ocrelizumab, and interferon beta-1a groups received ocrelizumab 600 mg; the 2000 mg group received 1000 mg. Our primary endpoint was the total number of ...
    16 Oct 2010
    Worryingly there was one death in the high dose Ocrelizumab group at 14 weeks, from "systemic inflammatory response syndrome". These very impressive results need to be tempered against the death that we must assume ...


    11 Nov 2012
    Rituximab, a monoclonal antibody that depletes B cells by targeting the CD20 molecule, has been shown to effectively reduce disease activity in MSers with relapsing MS as a single agent. Our investigator-initiated phase II ...
    04 May 2012
    B cells (cells that produce antibodies) have paradoxical roles in autoimmunity, exerting both pathogenic and protective effects. Pathogenesis may be antibody independent, as B cell depletion therapy (BCDT) leads to ...
    29 Jun 2011
    The investigators should be complemented for trying Rituximab in SPMS. In the past this is how therapies evolved; you started with an idea or scientific rationale and you then test the drug in an individual with the disease.
    08 Jun 2011
    Rituximab is a monoclonal antibody that targets a surface protein on B cells called CD20. There is good phase 2 data on its effectiveness when given intravenously (i.e. via a peripheral vein) in RRMS and a subgroup of PPMS ...


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