Sunday, 28 May 2017

Damaging Cholesterol

I recently asked how can statins work in secondary progressive MS.

In the absense of any real insight, I came up with a few ideas one of which was involving the cholesterol pathway to control/induce nerve damage

Bezine M, Debbabi M, Nury T, Ben-Khalifa R, Samadi M, Cherkaoui-Malki M, Vejux A, Raas Q, de Sèze J, Moreau T, El-Ayeb M, Lizard G. Evidence of K+ homeostasis disruption in cellular dysfunction triggered by 7-ketocholesterol, 24S-hydroxycholesterol, and tetracosanoic acid (C24:0) in 158N murine oligodendrocytes. Chem Phys Lipids. 2017 pii: S0009-3084(17)30011-7

Imbalance in the homeostasis of K+ ions has been reported to contribute to the pathogenesis of neurodegenerative diseases. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC), and tetracosanoic acid (C24:0), often found at increased levels in patients with Alzheimer's disease and Multiple Sclerosis, are able to trigger numerous nerve cell dysfunctions.  We therefore studied the impact of 7KC, 24S-OHC, and C24:0 on 158N mouse oligodendrocytes, and determined their impact on K+ homeostasis. The effects of 7KC, 24S-OHC and C24:0 on lipid membrane organization and membrane potential were examined. 7KC, 24S-OHC and C24:0 induced changes in lipid content and the cytoplasmic membrane. These events were associated with increased [K+]i. The positive correlation between [K+]i and cell death supports the potential involvement of K+ in 7KC-, 24S-OHC-, and C24:0-induced cytotoxicity.
Cholesterol can be oxidised to become agents called oxysterols (see the diagram above). These can bind to cells including oligodendrocytes and they can block the action of a number of ion channels including some potasium channels and also potassium and sodium exhangers. These cause a rise in the concentration of potassium within the cell, which eventually trigger the entry of calcium and the suicide of the cell. This is a mechanism of inducing cell death in oligodendrocytes as shown here, but probablyother cell types as well

Statins will get rid of the cholesterol and in doing so will remove oxysterols and so this damaging mechanism will not occur. Perhaps getting rid of some of the potassium from inside the cell may be a route to countering this problem. I could suggest how this appraoch may be achieved but that's another post.

Saturday, 27 May 2017

GABA and Remyelination-Its Confusing I know but no cause for concern

Yesterday I caused a bit of concern by a post on myelination as a GABA (inhibitory nerve transmitter) blocker stimulated developmental myelination, so people were worried about their GABA receptor stimulating drugs. Would they block repair? Answer is I do not definitively know but suspect not.

In contrast there could be implications that stimulation of GABA could save nerves. Again we don't have the data.

I will try explain a bit, but it is very, very complicated.

First things first, the report of GABAergic control of myelination is based on developmental myelination (myelinating nerves from the first time), and as the docs from Cambridge/Edinburgh have shown remyelination may not be the same process as developmental myelination.

Next it is far more complex than just GABA. What else has to be stimulated?

We have already been told that the oligodendrocyte precursor cells get stimulated by glutamate (excitatory nerve transmitter). This transmits their function via activity on glutamate receptors. Here there are lots of types, over twenty receptor genes.  There are three main ionotrophic (opens channels for electrically charged (ion) sodium calcium or potassium) subtypes AMPA, Kainate and NMDA binding subtypes

Myelination first acts via the AMPA sensitive variants, then their influence stops whilst the NMDA-sensitive subtypes come into play. This process will be influenced by the GABA receptors. This stimulates developmental maturation of the oligodendrocyte precursor cell and myelination of un-myelinated nerves. During this process the glutamate receptors and ion channels get down regulated. It is not the odd one, but loads of them.
Here are the potassium channels) or should I say some as I got bored and stopped at about M  ie. KCNM) but could have gone on eg N KCNN etc

Next there are more than one type of GABA receptor. There are two main types. One is GABA A and the other is GABAB. GABA A is an ionotrophic (via chloride) channel that can be stimulated by different types of drug as it has multiple sites and there are multiple genes making a multi-component receptor.

GABA B is a metabotrophic receptor which G protein coupled receptor that is linked signalling to control calcium channel activity and can signal via potassium channels.

Baclofen is the main GABA B receptor stimulator, used for spasticity. GABApentin, Pregabalin look like GABA but do not bind to the GABA receptors, although they may influence GABA production they act via ion channels to be ant-convulsants and pain controllers. The story about GABA and oligodendrocytes involved GABA A receptors, so the story is not about these drugs

Indeed in the experimental study they blocked the GABA response with a drug called Gabazine (SR-95531). It is used in scientific research and has no role in medicine, as it would be expected to produce convulsions. 

Any drug used in humans would never block the GABA A receptor to the extent used in the experiments so a block would never happen in humans. Experimental studies often use crazy doses of drugs to show a theorhectic possibility or define a mechanism. But they have no translational value. 

If the authors had read the ARRIVE guidelines about reporting experimental studies, they could have talked about the translatable aspects and if they had used clinical concentrations of GABA A blocking drugs, I bet they would have shown nothing...Nothing does not make for a good publication. But until this expriment is done, no cause for concern.

The importance of this post was to show that oligodendrocytes have ionotrophic function and they have loads of ion channels including loads of potassium channels.

#PatientSpeak: I have primary progressive MS ..........

I am preparing myself to let my patients with PPMS down. Are you? #PatientSpeak, #MSBlog #Ocrelizumab

I saw one of my patients the other day who has PPMS. His disability is worsening and clearly wants something done about it. He was very excited about the news that the FDA had licensed ocrelizumab for PPMS and wanted to know when ocrelizumab would be available under the NHS. I explained to him that ocrelizumab had yet to be licensed by the EMA and as the EMA tends to be more conservative than the FDA it wasn't certain by any means that it would be licensed in Europe for PPMS.  Even if ocrelizumab is licensed for PPMS, I suspect the EMA won't give it as broad a label as the FDA has done and may limit it to a particular population of pwPPMS. If this happens I informed this patient he may fall outside of the licensed indication, for example his PPMS may not be active enough. 

In addition, if and when the EMA licenses ocrelizumab for PPMS then NICE has to green-light it for use in the NHS. The latter may be a problem, particularly if ocrelizumab is priced to be cost-effective for RRMS. At the RRMS price NICE will need to compare it to best supportive care (no DMT) for PPMS and it is unlikely to be cost-effective using this comparator. I have been arguing for sometime now that this may be the time for Pharma to explore differential pricing and charge the NHS less when ocrelizumab is prescribed for PPMS. 

When I told this patient about the various hurdles that will need to be overcome for me to prescribe ocrelizumab for him he was very disappointed, so I asked him to put something down in words to start a conversation with other pwPPMS who live in Europe. 

Please note that Mark has given me permission to publish his name. In fact Mark sits on the Barts-MS Advisory Group and wrote a blog post on this in December 2015

A patient-with-PPMS's Perspective on Ocrelizumab

"Some 4 months after I was diagnosed with PPMS in May 2008, I remember speaking to a man who had had MS for a number of years and he said that I would be one of the lucky ones – there would be treatment for PPMS in the next ten years or so. I have always remembered this but of course with less and less conviction as the years have gone by. Now I think I will be just another of the countless unlucky ones, there will be no treatment for me.

So when Ocrelizumab was announced as a possible treatment for PPMS I was overjoyed and thought, you know, maybe he was indeed correct. However, as ever with this disease any joy is always mixed with disappointment and so it was when I discovered that I was too old to be considered for the trial – I was 57. This was a bitter disappointment as I do not consider myself to be old, let alone too old. Indeed I have taken part in 3 trials since being diagnosed, I am generally fit, look after myself, lost weight, go to the physio twice weekly and maintain a good positive outlook. I do “my bit” but, there you are, I am too old.

Following the Ocrelizumab trials I like others with PPMS are very keen for the drug to licensed as currently it is our only hope. I understand that whilst it is not particularly effective where MS has taken a hold - eg on the lower limbs, it is effective on the upper limbs. For this reason alone it should be prescribed as our upper limbs must be saved they act as our legs by allowing us to use a stick and maintain some independence by using mobility scooters and other aids. Once our arms are as stiff as our legs we are effectively quadriplegic - if that can be avoided or at least delayed then surely we should have the drug. After all if there was a cancer treatment that whist not effective on the primary tumour but reduced or delayed the spread of secondary tumours, I am sure that would be licensed."

Mark Harrington, May 2017, London

Friday, 26 May 2017

#BrainHealth: a brain health guide for nurses

CMSC launch of our #BrainHealth guide for MS nurse specialists. #CMSC2017 

The main focus of the CMSC meeting is CME (continuing medical education) for allied medical professionals in particular MS clinical nurse specialists. For this reason we have used this meeting to launch our Brain Health guide for MS specialist nurses, or nurse practitioners as they are frequently referred to in the US. Please download the guide, read it and use it in your clinical practice. 

Jodi Haartsen
MS Brain Health Champion & MS Nurse Practitioner extraordinaire, 

on our Brain Health stand at the CMSC in New Orleans.

CoI: multiple

First case of PML on Ocrelizumab reported

We have been saying one of the important considerations when starting treatment is how do you switch off your drug, we reported rebound after fingolimod and this is a well known problem with Natalizumab. PML is the other major problem with natalizumab.

The first case of PML on ocrelizumab has been reported. Again one suspects that subclinical PML due to natalizumab was the problem. According to Media the case occurred in a JC virus-positive pwMS who had stopped taking natalizumab in February after being on the drug for three years, and switched to ocrelizumab with a first dose given in April. Ocrelizumab is not licenced within Europe but it was apparently used in Germany where the case occurred.

ProfG will no doubt get the details, but perhaps not the news you want when going to the regulators to get approval for use in Europe.

GABA controls oligodendrocytes

Hamilton NB, Clarke LE, Arancibia-Carcamo IL, Kougioumtzidou E, Matthey M, Káradóttir R, Whiteley L, Bergersen LH, Richardson WD, Attwell D. Endogenous GABA controls oligodendrocyte lineage cell number, myelination, and CNS internode length. Glia. 2017;65(2):309-321

Adjusting the thickness and internodal length of the myelin sheath is a mechanism for tuning the conduction velocity of axons to match computational needs. Interactions between oligodendrocyte precursor cells (OPCs) and developing axons regulate the formation of myelin around axons. We now show, using organotypic cerebral cortex slices from mice expressing eGFP in Sox10-positive oligodendrocytes, that endogenously released GABA, acting on GABAA receptors, greatly reduces the number of oligodendrocyte lineage cells. The decrease in oligodendrocyte number correlates with a reduction in the amount of myelination but also an increase in internode length, a parameter previously thought to be set by the axon diameter or to be a property intrinsic to oligodendrocytes. Importantly, while TTX block of neuronal activity had no effect on oligodendrocyte lineage cell number when applied alone, it was able to completely abolish the effect of blocking GABAA receptors, suggesting that control of myelination by endogenous GABA may require a permissive factor to be released from axons. In contrast, block of AMPA/KA receptors had no effect on oligodendrocyte lineage cell number or myelination. These results imply that, during development, GABA can act as a local environmental cue to control myelination and thus influence the conduction velocity of action potentials within the CNS.

GABA is the major inhibitory neurotransmitter and blocks signals from excitatory nerves such as glutamate. A few years ago, it was found that oligodendrocyte precursors have glutamate receptors and when these get stimulated it probably acts as a signal to the oligodendrocyte precursor cells to change into an oligodendrocyte and to start myelination. The glutamate is essentially a calcium channel making the inside of the  cell more electrically positive. however blocking this made no infuence on cell numbers. However, if you stimulate with GABA A which is a chloride channel meaning the inside becomes more electrically negative you get less oligos and less myelination. Is there any evidence that benzodiazepines block or stimulate myelination ?  Don't think so, but have people looked ?. 

Thursday, 25 May 2017

#NewsSpeak: Jet-lag and the CMSC 2017 meeting in New Orleans

Jet-lagged, tired and MSed-out in New Orleans; time to take a break? #CMSC2017 #MSBlog #NewsSpeak

I arrived late last night in New Orleans and will be talking at a teaching session this morning. The main objectives of my talk are:
  1. MS is 1 and not 2, 3 or 4 diseases
  2. MS is a length-dependent axonopathy 
  3. Progressive MS is a tractable problem
  4. Neuro-repair is feasible and provides hope for the future
  5. Holistic management of MS#
I am very jet-lagged and tired. I have less than 3 hours sleep on top of several weeks of sleep deprivation. I was meant to be flying back this evening to travel to Scotland for a week's walking holiday doing the Cape Wrath trail. But had to pull out of the walk because of my hip problem; I simply can't do 100+ miles carrying a 20+ kg backpack. I was really looking forward to some time out, but instead my supposed week-off has already filled up rapidly with MS-related activities. I reopened my NHS clinic,  have scheduled several meetings including attending an important biomarker meeting.

The one positive thing about a long trans-Atlantic flight is that I managed to finish 9 writing tasks with plenty more to do. Hopefully, I will be able to maximise some of my free time in New Orleans and next week to complete some more tasks. The life of an academic is no different to any other; we are on a treadmill that seems to be going faster and faster.  

The following is my talk that I will be giving this morning, the programme for the CMSC meeting and a satellite I have been asked to chair are below. Regarding the latter  the previous chair was unable to attend the meeting. The satellite is being hosted by 'MS in the 21st Century' an initiative that focuses on patient engagement. It should be good so if you are in New Orleans please come along. In addition, I am presenting several abstracts and have done already done a Medscape panel discussion.  

CoI: multiple


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May 2017

Letter from the President

Welcome to the second ECTRIMS newsletter of 2017. Being already in the month of May, I begin by highlighting that this year's World MS Day is May 31st. World MS Day is an excellent initiative of the MS International Federation and its members to raise awareness of MS throughout the world. For further information see (

Plans continue to proceed well for this year's Congress (MSParis2017). As happens every three years, the meeting this year is being held jointly with ACTRIMS. It will be the 7th such joint meeting and will take place in Paris on October 25th - 28th. Comprehensive Scientific and Teaching Course Programmes have been established and further details of these are available on the website, along with other  information relevant to the meeting ( The deadline for abstract submission is May 31st. This year, ECTRIMS will be providing a limited number of rooms at a very reduced rate for non-profit, non-governmental specialty groups or organisations in the MS field that may want to hold a meeting at the time of the Congress. For further information, see (

ECTRIMS keeps busy with a number of regular activities other than the annual Congress. This year's Focused Workshop on the topic of "Advancing Trial design in MS" was held in Rome in March in association with the Progressive MS Alliance. It was a very successful, informative and interactive two-day meeting. This month (May 2017), the third ECTRIMS Regional Teaching Course was successfully held in Vilnius, in conjunction with the Baltic MS council. In June, the 5th ECTRIMS Annual Summer School, which is on "Rehabilitation and Symptomatic Treatment in MS", will take place in Santiago de Compostela. The summer school programme and faculty will provide an excellent educational experience for the attendees. Plans are already underway to hold further Regional Teaching Courses in 2018, along with a Focused Workshop and Summer School. Warmest thanks to all my Executive Committee colleagues for their leadership for taking forward these activities.

The 2017 round of ECTRIMS fellowship awards was recently decided. There were many very good applications this year and a total of 10 fellowships have been awarded as follows: Post-doctoral Research Exchange Fellowship (4), Clinical Training Fellowship (3), ECTRIMS-MAGNIMS Fellowship (2) and MS Nurse Training Fellowship (1). Elsewhere in the newsletter you will find reports from several previously awarded fellows.

I hope you find this newsletter enjoyable and informative.
David Miller


World MS Day 2017

What is World MS Day?
World MS Day, which will occur on May 31st this year, brings the global MS community together to share stories, raise awareness and campaign with and for everyone affected by multiple sclerosis. World MS Day is the only global awareness raising campaign for MS. Every year, the MS movement comes together to provide public with information about MS and to raise awareness on how it affects the lives of more than 2.3 million people around the world.
In 2017, the theme for World MS Day is "Life with MS". As life with MS can be difficult and each day brings its new challenges, valuable tips for living well with MS will be made available.
Since its inception in 2009, the World MS Day has grown from strength to strength, reaching hundreds of thousands of people in more than 78 countries worldwide and continuing to grow every year.
How can you get involved?
Read more about World MS Day at and learn about how you can take part in the World MS Day.

ECTRIMS Focused Workshop 2017/ 9-10 March 2017 in Rome, Italy

The ECTRIMS 2017 Focused Workshop took place on March 9th and 10th in Rome. The topic was "Advancing Trial Design in Progressive MS" and it was held in association with the International Progressive MS Alliance. There were about 50 participants encompassing a broad range of expertise, including clinical neurology, neuropathology, trial design, statistical, pharmaceutical, regulatory and lay viewpoints. Themes included treatment targets; trials to date; clinical outcome measures; interim outcome measures focused on neuroprotection that included MRI, OCT, CSF, neurophysiology and PET;   trial designs and statistical analysis; insights from big datasets and ongoing phase 2 trials; and pharmaceutical and regulatory considerations. There were didactic presentations and ample time was allocated for round table and open discussions. The workshop covered a lot of ground and there were many lively discussions. It is proposed that the proceedings will be published as a series of short papers in a themed issue of the Multiple Sclerosis Journal with authors coming from amongst the workshop attendees. We thank Jeremy Chataway and Bob Fox for being the guest editors on this publication.

ECTRIMS Regional Teaching Course 2017/ 11-12 May 2017 in Vilnius, Lithuania

ECTRIMS regional teaching courses have been established in 2016. After two successful teaching courses in St.Petersburg/Russia and Dubai last year this educational activity continued this year with the third teaching course in Vilnius/Lithuania. The course was organized by the ECTRIMS Teaching Course Committee in close collaboration with the Baltic Neurological community. The programme covered basic aspects of MS like the involvement of genes and environmental factors in the pathogenesis of MS and the immunopathophysiology of MS. The main focus of the teaching course was practice relevant topics including differential diagnosis, treatment monitoring and discussions about the rationale for switching or escalating therapies. The teaching course was well attended with 90 participants. The active interaction and high quality of the presentations made this teaching course again a great success, which is also exemplified by a very positive feedback from the participants.
For further information on upcoming teaching courses and detailed programme please visit the ECTRIMS Website here.

ECTRIMS Summer School 2017 / 13 - 15 June 2017 in Santiago de Compostela, Spain

The 2017 ECTRIMS Summer School on "Rehabilitation and symptomatic treatment in multiple sclerosis", organized in collaboration with RIMS, will take place in Santiago de Compostela, Spain, on June 13th – 15th.
The target audience is represented  by high-potential young researchers and clinical experts from different backgrounds (neurologists, rehabilitation physicians and multi-disciplinary therapy team) who want to generate and implement best evidence-based treatment and rehabilitation care.
Through formal presentations delivered by international experts,  interactive, multidisciplinary group discussions and multi-disciplinary group work on research projects,  this course will provide an update on the framework of rehabilitation and available evidence for the effectiveness of motor and cognitive, as well as emotional symptomatic treatment and rehabilitation interventions in MS. Moreover, it will cover epidemiology, physiopathology, diagnosis and evidence base behind the various pharmacologic and non-pharmacologic approaches to the management of MS symptoms, which in most cases requires multidisciplinary input. The course will pursue as main learning objectives understanding the indications and concepts of symptomatic treatment and rehabilitation, and its effects on the patient everyday functioning, integrating evidence from multiple disciplines into clinical case management and identifying key research questions and challenges for clinical implementation of holistic symptomatic treatment and rehabilitation.

ECTRIMS Fellowship 2017

ECTRIMS offers a comprehensive range of fellowship programmes for different target groups.
In 2017 10 new fellowships were awarded:
Dr. Gloria Castellazzi (Italy): 2-year fellowship at UCL Institute of Neurology, Queen Square MS Centre, Department of Neuroinflammation, London, United Kingdom, under mentorship of Prof. Claudia Gandini Wheeler-Kingshott. Project: Developing a clinical decision system based on characterising shared and specific functional features of MS subtypes.
Dr. Joanna Marczynska (Poland): 2-year fellowship at University of Southern Denmark, Neurobiology, Odense C, Denmark, under the mentorship of Prof. Trevor Owens. Project: Mechanisms suppressing autoimmune responses in the central nervous system.
Dr. Kyla McKay (Canada): 2-year fellowship at the Karolinska Institutet, Clinical Neuroscience, Stockholm, Sweden, under the mentorship of Prof. Jan Hillert. Project: The causes and consequences of paediatric multiple sclerosis: A population-based study.
Dr. Emanuela Oldoni (Italy): 2-year fellowship at KU Leuven, Department of Neurosciences, Leuven, Belgium, under the mentorship of Prof. An Goris and Prof. Bénédicte Dubois. Project: Multiple sclerosis heterogeneity: patient-to-patient variation in cerebrospinal fluid biomarkers
Dr. Nuria Cerdà Fuertes (Spain): 1-year clinical training fellowship at the University Hospital Basel, Neurologisch-Neurochirurgische Poliklinik, Basel, Switzerland, under the mentorship of Prof. Tobias Derfuss. Project: Evaluation of clinical bedside tests (primitive reflexes e.g. palmomental reflex) of MS patients in correlation with neuropsychological tests.
Dr. Giordani dos Passos (Brazil): 1-year clinical training fellowship at the University of Oxford, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford, United Kingdom, under the mentorship of Prof. Jacqueline Palace. Project: Are there differences in MS severity, as assessed by MRI and clinical parameters, between different racial and ethnic groups?
Dr. Pietro Maggi (Belgium): 1-year clinical training fellowship at the Lausanne University Hospital, Department of Neurology, Lausanne, Switzerland, under the mentorship of Prof. Renaud Du Pasquier. Project: High field gradient echo MRI enhances the differentiation between multiple sclerosis and other inflamatory disorders: a further step beyond the concept of "no better explanation".
Macarena Rus Hidalgo (Spain): 6-months fellowship at the IRCCS Foundation Carlo Besta Neurological Institute, Neurology 4 Unit-neuroimmunology and neuromuscular disorders, Milan, Italy, under the mentorship of Prof. Prof. Silvia Rossi. Project: A multicentric randomized PRAGmatic trial to compare the effectiveness of fingolimod versus
dimethyl‐ fumarate on patient overall disease experience in relapsing remitting Multiple
Sclerosis: novel data to inform decision‐makers – (PRAG‐MS).
Dr. Soheil Damangir (Sweden): 1-year fellowship at the VU University Medical Center, Amsterdam, Netherlands, with collaboration at the Vall d'Hebron University Hospital, Barcelona, Spain under the mentorship of Dr. Vrenken and Prof. Barkhof. Project: Optimizing crowd-sourced solutions toward generating large reference datasets for WM lesion segmentation in MS.
Dr. Marcello Moccia (Italy): 1-year fellowship at the UCL Institute of Neurology, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom under the mentorship of Prof. Ciccarelli and Prof. Barkhof. Project: Improving longitudinal spinal cord atrophy measurements for clinical trials in multiple sclerosis by using the Generalised Boundary Shift Integral (GBSI).

MSIF-ECTRIMS McDonald Fellowship

Starting in 2016, MSIF (Multiple Sclerosis International Federation) and ECTRIMS jointly support a 2-year McDonald fellowship every year. This fellowship is offered to young researchers from emerging countries and enables the recipient to travel to an established research institution anywhere in the world to work with leading researchers in the field of MS. It is intended that these fellows return to their home countries after finishing the fellowship program to establish their own research using the newly learned techniques.
For more information regarding the fellowship program and for application please visit the MSIF webpage:
Application deadline: 30 June 2017

Reports of ECTRIMS Fellows


Ana Luisa Falcão PhD – 2015 Awardee
Research Topic
Epigenetic states underlying oligodendrocyte precursor differentiation in Multiple Sclerosis
Fellowship Institution
Karolinska Institute, Department of Medical Biochemistry and Biophysics, Stockholm, Sweden
Dr. Gonçalo Caselo-Branco
Fellowship Duration
2 years
Summary as ECTRIMS Postdoctoral Research Exchange Fellow 2015 - 2017
The research objective of this fellowship project was to understand the epigenetic mechanisms underlying oligodendrocyte precursor cell (OPC) differentiation during development and in Multiple Sclerosis (MS). In the first part of the project we investigated the role of citrullination in oligodendrocyte (OL) differentiation and myelin maintenance. Citrullination is the conversion of an arginine to the neutral citrulline, a process mediated by Peptdidylarginine Deiminases (Padi) and found induced in MS. We have uncovered the PADI2-mediated citrullination targets in OLs and found that both cytoplasmic and nuclear proteins are citrullinated, such as myelin proteins and histones. Our study shows that PADI2 citrullination impacts on proper OL development acting as an epigenetic regulator through histone citrullination, but also displays other functions in the cytoplasm and myelin as observed by its interaction with several myelin proteins. In a second part of the project we have performed single cell sequencing profiling in OL lineage cells isolated from the brain and spinal cord of the MS mouse model EAE, and from healthy controls. We observed a remarkable segregation between cell populations from controls and diseased animals that discloses many targets of the disease.
We are currently preparing the 2 manuscripts describing the findings from these projects and we have recently published part of the results from the single cell RNA-seq profiling in OLs (Marques et al, Science).


María Isabel Zuluaga MD – 2015 Awardee
Research Topic
The effect of hormonal changes on women MS risk and prognosis
Fellowship Institution
Centro de Esclerosis Mútiple de Catalunya – CEMCat, Barcelona, Spain
Dr. Mar Tintoré 
Fellowship Duration
6 months
Summary as ECTRIMS Clinical Training Fellowship Programme Fellow 2015
I developed my ECTRIMS Clinical training fellowship at the CEMCat. During these months, I participated in activities of patient care and clinical research. My project was to investigate the possible association of reproductive background, hormonal changes and environmental factors in the risk and prognosis of MS. We found that age at menarche was not associated with an early CIS, neither with the risk of second attack or accrual disability. We also found that pregnancy before or after CIS did not modify the risk of CDMS or accrual disability. Regarding environmental factors, we found that vitamin D deficiency and smoking are risk factors for disability progression in the BARCELONA CIS cohort.
I´m very thankful with ECTRIMS, my mentors and co-workers at CEMCat; this experience had enriched my professional and personal life, and also will positively impact the care of MS patients back in my country.


Arman Eshaghi MD, PhD – 2015 Awardee
Research Topic
"To explore imaging phenotypes of patients with multiple sclerosis using 4-dimensional voxel-based morphometry"
Fellowship Institution
UCL Institute of Neurology, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom
Prof. Olga Ciccarelli
Fellowship Duration
1 year
Summary as ECTRIMS MAGNIMS Fellowship in Magnetic Resonance Imaging in MS Fellow 2015 - 2016
During my ECTRIMS-MAGNIMS fellowship, I collected a big dataset of more than a thousand patients with multiple sclerosis, who have been followed longitudinally. I looked at the temporal and spatial evolution of brain atrophy. I looked at the differences of atrophy across neuroanatomical regions in multiple sclerosis phenotypes, and baseline imaging markers to predict disability accumulation in advance of time. This fellowship allowed me to work in a truly multidisciplinary environment, where I worked in between the UCL Institute of Neurology and UCL Department of Computer Science to learn computational methods and apply them in neurology. I presented my work as a platform presentation during ECTRIMS 2016 in London and was awarded "the Best Oral Presentation Given by a Young Investigator". I have prepared the results of my fellowship as a manuscript, which is now submitted and is under peer review.

Meeting Dates

ECTRIMS Summer School 2017
Santiago de Compostela / Spain: 13 – 15 June 2017
MSParis2017 - 7th Joint ECTRIMS - ACTRIMS Meeting
Paris / France: 25 – 28 October 2017
Berlin / Germany: 10 - 12 October 2018
We are looking forward to seeing you in Paris!

Please be aware of fraudulent organisations!

There are an increasing number of fraudulent websites that impersonate MSParis2017. We would like to alert all participants to be aware of possible scams and to strongly advise you to only use the official MSParis2017 registration and ECTRIMS accommodation agency Congrex Travel.
ECTRIMS Executive Committee
D. Miller, London/UK, President
B. Hemmer, Munich/DE, Vice President
M. P. Amato, Florence/IT, Secretary
T. Derfuss, Basel/CH, Treasurer & Newsletter Editor
M. Tintoré, Barcelona/ES
S. Vikusic, Lyon/FR
L. Brundin, Stockholm/SE