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1  Hoito / Lääkitys / Re: Lemtrada
 Pvm: 16.06.2019 - 19:01:07 
Keskustelun aloitti tui | Kirjoittaja Red Kite  
Käypä hoidon sivuille on ilmestynyt EMA:n varoitus Lemtradasta.

"Euroopan lääkevirasto (EMA) on aloittanut 4/2019 alemtutsumabin turvallisuusarvioinnin. Siihen on yhdistetty muun muassa sydän- ja verisuoni- sekä immuunijärjestelmän toimintaan liittyviä haittoja, ja myös joitakin kuolemantapauksia on raportoitu näihin liittyen.

   EMA suosittelee, että arvioinnin aikana alemtutsumabia käytetään vain potilailla, joiden MS-tauti on erittäin aktiivinen kahden taudin kulkua muuntavan lääkkeen käytöstä huolimatta, tai silloin kun muita taudin kulkuun vaikuttavia lääkkeitä ei voida käyttää."


2  Yleinen / MS-diagnoosi / PPMS-diagnoosi ja Ocrevus
 Pvm: 31.05.2019 - 15:15:00 
Keskustelun aloitti Haikara | Kirjoittaja Haikara  
Hei kaikki, kirjoitan tänne ensimmäistä kertaa!
Olen vast'ikään saanut ppms-diagnoosin ja minulle on tarjottu Ocrevus-hoitoa. Tässä onkin ollut pohtimista ja pureskeltavaa molempien asioiden osalta.
Ensioireeni alkoivat reilu pari vuotta sitten oikean jalan läpsymisenä väsyneenä. Kun oireet viime syksynä olivat edenneet siihen pisteeseen etten enää pystynyt juoksemaan edes paria metriä, menin työterveyslääkärille. Aika pian tutkimukset siirtyivät HUS:iin ja nyt olen talven aikana käynyt neljässä mk-kuvauksessa, likvorissa ja vaikka kuinka monessa verikokeessa. Magneettikuvissa oli runsaat löydökset sekä aivoissa että selkäytimessä, muutama plakeista oli voimistuvia. Myös likvorin IgG oli koholla. Diagnoosi (silloin jo odotettu) oli valmis huhtikuussa; rrms. Minut otettiin melkein heti sisään kortisonipulssiin.
Tästä ei ollut apua, enkä ollut kokenut että oireistoni olisi aaltoilevaa.
Tapaukseni meni ms-työryhmän käsittelyyn spinaalisten löydösten, aaltoilevuuden puute sekä korkea ikäni (55v) ja tulii takaisin muodossa ppms.

Tässä on ollut paljon pohdittavaa viime viikkoina, sekä diagnoosin että tulevan hoidon suhteen. Aluksi ajatukset ovat kieräneet kehää tuon Ocrevuksen suhteen. Pelkään haittavaikutuksia, mutta vaihtoehtoisia lääkkeitä ei ole ppms:ään. Nyt olen kääntymässä hoidon aloittamisen puoleen koska vointi ei saisi laskea ainakaan kovaa vauhtia alaspäin. Epävarma

Kyselenkin onko täällä parliksessa Ocrevuksen käyttäjiä ja mikä on teidän kokemus tästä lääkkestä?



3  Tutkimus / Tutkimus / Re: Synteettinen molekyyli voi korjata myeliiniä
 Pvm: 23.05.2019 - 11:28:58 
Keskustelun aloitti HopeSprings | Kirjoittaja Neilikkamies  
Tässä on kolmas säätiö mainitun kahden liäksi, joka on rahoittanut tutkimusta: Race to Erase MS Is Making Strides in Expanding MS Treatments.

Hyvä, että tutkimus etenee myös ilman lääkefirmojen kiinnostusta. Voisi jopa epäillä, että isot MS-lääkefirmat eivät halua kehittää lääkettä, joka toimii liian hyvin ja syö kalliden lääkkeiden myyntituloja.

4  Tutkimus / Tutkimus / Re: Krooniset bakteeri-infektiot
 Pvm: 21.05.2019 - 13:02:07 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Humoral response to EBV is associated with cortical atrophy and lesion burden in patients with MS

https://nn.neurology.org/content/3/1/e190

January 7, 2016
Abstract

Objective: Because dysregulated Epstein-Barr virus (EBV)-infected B cells may induce meningeal inflammation, which contributes to cortical pathology in multiple sclerosis (MS), we investigated associations between antibody responses to EBV and development of cortical pathology in MS.

Methods: We included 539 patients with MS (369 with relapsing-remitting MS, 135 with secondary progressive MS, and 35 with primary progressive MS), 66 patients with clinically isolated syndrome (CIS), 63 patients with other neurologic diseases (OND), and 178 age- and sex-matched healthy controls (HC). All participants were scanned on 3T MRI. Serum samples were analyzed for IgG antibodies against EBV viral capsid antigen (VCA) and EBV nuclear antigen-1 (EBNA-1), and their quartiles were determined on the whole study sample. Differences between the study groups were assessed using analysis of covariance adjusted for multiple comparisons.

Results: More than 30% of patients with MS and CIS presented with the highest quartile of anti-EBV-VCA and -EBNA-1 status compared to ≤10% of HC (p < 0.001). The figures were 9 (14.3%) and 7 (12.3%) for patients with OND. Patients with MS with the highest quartile of anti-EBV-VCA showed significantly increased T2 lesion volume (p = 0.001), T1 lesion number (p = 0.002), and T1 lesion volume (p = 0.04) and decreased gray matter (p = 0.041) and cortical (p = 0.043) volumes compared to patients with MS with lower quartiles. No significant differences of MRI outcomes in patients with CIS, patients with OND, and HC with lower or highest quartiles of anti-EBV-VCA and -EBNA-1 were detected.

Conclusions: Humoral response to anti-EBV-VCA and -EBNA-1 is associated with more advanced cortical atrophy, accumulation of chronic T1 black holes, and focal white matter lesions in patients with MS.

5  Tutkimus / Tutkimus / Synteettinen molekyyli voi korjata myeliiniä
 Pvm: 18.05.2019 - 23:30:58 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Study shows promise in repairing damaged myelin

https://www.sciencedaily.com/releases/2019/04/190418141614.htm

April 18, 2019

A scientific breakthrough provides new hope for millions of people living with multiple sclerosis. Researchers at Oregon Health & Science University have developed a compound that stimulates repair of the protective sheath that covers nerve cells in the brain and spinal cord.

The discovery, involving mice genetically engineered to mimic multiple sclerosis, published in the journal JCI Insight.

MS is a chronic condition that affects an estimated 2.3 million people worldwide. In MS, the sheath covering nerve fibers in the brain and spinal cord becomes damaged, slowing or blocking electrical signals from reaching the eyes, muscles and other parts of the body. This sheath is called myelin. Although myelin can regrow through exposure to thyroid hormones, researchers have not pursued thyroid hormone therapies due to unacceptable side effects.

Although several treatments and medications alleviate the symptoms of MS, there is no cure.

"There are no drugs available today that will re-myelinate the de-myelinated axons and nerve fibers, and ours does that," said senior author Tom Scanlan, Ph.D., professor of physiology and pharmacology in the OHSU School of Medicine.

Co-author Dennis Bourdette, M.D., chair of neurology in the OHSU School of Medicine and director of the OHSU Multiple Sclerosis Center, said he expects it will be a few years before the compound advances to the stage of a clinical trial involving people. Yet the study provides fresh hope for patients in Oregon and beyond.

"It could have a significant impact on patients debilitated by MS," Bourdette said.

The discovery, if ultimately proven in clinical trials involving people, appears to accomplish two important goals:

   Myelin repair with minimal side effects: The study demonstrated that the compound -- known as sobetirome -- promotes remylenation without the severe side effects of thyroid hormone therapy. Thyroid hormone therapy has not been tried in people because chronic elevated exposure known as hyperthyroidism harms the heart, bone, and skeletal muscle.
   Efficient delivery: Researchers developed a new derivative of sobetirome (Sob-AM2) that penetrates the blood brain barrier, enabling a tenfold increase in infiltration to the central nervous system.

"We're taking advantage of the endogenous ability of thyroid hormone to repair myelin without the side effects," said lead author Meredith Hartley, Ph.D., an OHSU postdoctoral researcher in physiology and pharmacology.

Co-authors credited the breakthrough to a collaboration that involved scientists and physicians with expertise ranging across neurology, genetics, advanced imaging, physiology and pharmacology.

One patient said the research could be a "total game-changer" for people with MS.

Laura Wieden, 48, has lived with multiple sclerosis since being diagnosed in 1995. The daughter of Portland advertising executive Dan Wieden, she is the namesake and board member of the Laura Fund for Innovation in Multiple Sclerosis, which funded much of the research involved in the study published today.

"I am really optimistic," Wieden said. "I hope that this will be literally a missing link that could just change the lives of people with MS."

Scanlan originally developed sobetirome as a synthetic molecule more than two decades ago, initially with an eye toward using it to lower cholesterol. In recent years, Scanlan's lab adapted it as a promising treatment for a rare metabolic disease called adrenoleukodystrophy, or ALD.

Six years ago, Bourdette suggested trying the compound to repair myelin in MS.

Supported by funding provided through the Laura Fund and the National Multiple Sclerosis Society, the team turned to Ben Emery, Ph.D., an associate professor of neurology in the OHSU School of Medicine. Emery, an expert who previously established his own lab in Australia focused on the molecular basis of myelination, genetically engineered a mouse model to test the treatment.

With promising early results, researchers wanted to see if they could increase the amount of sobetirome that penetrated into the central nervous system.

They did so through a clever trick of chemistry known as a prodrug strategy.

Scientists added a chemical tag to the original sobetirome molecule, creating an inert compound called Sob-AM2. The tag's main purpose is to eliminate a negative charge that prevents sobetirome from efficiently penetrating the blood-brain barrier. Once Sob-AM2 slips past the barrier and reaches the brain, it encounters a particular type of brain enzyme that cleaves the tag and converts Sob-AM2 back into sobetirome.

"It's a Trojan horse type of thing," Scanlan said.

Researchers found that the treatment in mice not only triggered myelin repair, but they also measured substantial motor improvements in mice treated with the compound.

"The mouse showed close to a full recovery," Scanlan said.

Scientists say they are confident that the compound will translate from mice to people. To that end, OHSU has licensed the technology to Llama Therapeutics Inc., a biotechnology company in San Carlos, California. Llama is working to advance these molecules toward human clinical trials in MS and other diseases.

Bourdette said even though it may not help his patients today, he's optimistic the discovery eventually will move from the lab into the clinic.

"Right now, what it means is hope," he said.


6  Tutkimus / Tutkimus / Re: Krooniset bakteeri-infektiot
 Pvm: 18.05.2019 - 23:17:49 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Atara Biotherapeutics Study Links Epstein-Barr Virus Infection with MS

https://multiplesclerosisnewstoday.com/2018/06/19/atara-biotherapeutics-study-li...
nks-epstein-barr-virus-infection-with-ms/

Analysis of post-mortem brain samples from multiple sclerosis (MS) patients and healthy individuals (without neurologic disease) showed that while signs of Epstein-Barr virus (EBV) infection are present in both groups of brains, EBV-positive immune cells were more prevalent and densely populated in the MS brain.

The study reporting those findings, “Molecular signature of Epstein-Barr virus infection in MS brain lesions,” was published in the journal Neurology: Neuroimmunology & Neuroinflammation, the official journal of the American Academy of Neurology.

EBV infection is estimated to affect about 95% of adults worldwide, and previous studies have suggested a potential causal link between EBV infection and the risk for MS. These studies reported that MS patients had higher levels of antibodies against EBV than non-MS individuals, but follow-up studies have failed to find the same results.

Now, researchers analyzed autopsied brain samples from a MS brain tissue bank and from healthy, non-MS samples (controls).

They detected signs for the presence of EBV in 93% of MS brain samples, but also in the controls, although to a less extent (78%).
******

EBV infects immune B-cells, and the results showed that 85% of MS brain samples contained a higher percentage of B-cells positive for EBV-encoded RNA. In contrast, almost none of these cells were found in brain samples from controls.

“The Neurology publication extends the growing body of evidence linking EBV infection and MS using a well-characterized MS brain tissue bank,” Chris Haqq, MD, PhD, said in a press release. Haqq is executive vice president of research and development and chief scientific officer of Atara Biotherapeutics.

“We observed that EBV is present in both MS and control brains, with EBV-infected B-cells and plasma cells more prevalent and localized to MS brain lesions,” Haqq said.

Within immune B-cells, EBV switches between latent and lytic forms. The latent form is a way for the virus to evade the host’s immune system, whereas the lytic form corresponds to a state in which the virus replicates more actively. EBV infection was detectable in both MS and non-MS brains. although latent virus was more prevalent in MS brains, and lytic virus was restricted to chronic MS lesions.

“Taken together, our results that are derived from a well-characterized MS brain tissue bank support previous studies demonstrating the presence of EBV in the MS brain,” the team concluded.

“These findings advance the understanding of EBV’s potential role in MS pathogenesis and provide support for targeting EBV-infected immune cells associated with chronic MS lesions as a potential treatment for this severe autoimmune disorder,” Haqq said.

Atara is developing two therapies, ATA188 and ATA190, to eliminate EBV-infected  B-cells in the central nervous system that can induce autoimmune responses and potentially contribute to MS development. Early results suggest these therapies can induce clinical improvements in MS symptoms.

7  Tutkimus / Tutkimus / Re: Krooniset bakteeri-infektiot
 Pvm: 18.05.2019 - 23:11:51 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Multiple sclerosis: Discovery of a mechanism responsible for chronic inflammation

https://www.sciencedaily.com/releases/2019/05/190510091354.htm

May 10, 2019
Multiple sclerosis (MS) is an autoimmune disease. The defense system that usually protects patients from external aggression turns on its own cells and attacks them for reasons that are not yet known. Scientists from the Institut Pasteur have shown that ancient viruses are involved in the acute inflammatory defense response that may contribute to the disease.

Multiple sclerosis (MS) is an incurable inflammatory autoimmune disease that leads to irreversible damage to the brain and spinal cord. This disease is also associated with the reactivation of ancient viruses, which were inserted in our DNA during the evolution of humankind. It was therefore long thought that multiple sclerosis was due to a viral infection.

"Our study shows that reactivation of ancient viruses does not correspond to an infectious phenomenon, but to a defense response of the body when faced with an acute inflammatory phenomenon" explains Christian Muchardt, Head of the Epigenetic Regulation Unit at the Institut Pasteur.

Viral sequences were neutralized during evolution and no longer represent a source of infection. But these sequences are a source of external DNA containing information about virus behavior. Cells have therefore been able to control these sequences to detect infections as quickly as possible and turn on their defense genes during an attack.

These viral sequences are, above all, used to control defense genes in stem cells. They lie dormant in adult cells and it is the more traditional sequences that become active. By examining samples from patients with MS, the scientists observed that regulatory sequences of viral origin emerged from their dormant state and were responsible for abnormal expression of several pro-inflammatory genes.

To conclude, in multiple sclerosis, activation of viral sequences does not correspond to an infectious phenomenon but to the unexpected use of regulatory sequences, leading to chronic excessive inflammation.

"The discovery of this mechanism, linked to epigenetic phenomena, may one day pave the way for management of MS using small molecules that inhibit chromatin modification enzymes" sums up Christian Muchardt.



8  Tutkimus / Tutkimus / Re: Suolistobakteerit, myeliini ja aivotoiminta
 Pvm: 18.05.2019 - 22:53:43 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Discovery of long-lived macrophages in the intestine

https://www.sciencedaily.com/releases/2018/08/180830113017.htm

August 30, 2018

Macrophages are specialised immune cells that destroy bacteria and other harmful organisms. KU Leuven scientists, Belgium, have come to the surprising conclusion that some macrophages in the intestines of mice can survive for quite some time. Most importantly, these long-lived macrophages are vital for the survival of the nerve cells of the gastrointestinal tract. This sheds new light on neurodegenerative conditions of the intestine, but also of the brain.

In the immune system macrophages play the role of PacMan: they are white blood cells that clean up foreign substances by engulfing them. Apart from this, macrophages themselves provide vital growth factors and support for different tissues in the body, allowing them to function and develop properly. As such, these specialised immune cells are soldier and nourisher at the same time. Their proper functioning is immensely important in the intestine, as they have to differentiate between harmful bacteria, harmless bacteria and nutritional components.

Scientists assumed that macrophages in the intestine are short-lived and live for about three weeks at most in both mice and humans before being replaced by new cells. A KU Leuven study now shows that this is not entirely true, explains Professor Guy Boeckxstaens. "We've discovered that a small part of the macrophages in mice is long-lived. We marked certain macrophages and found that they still functioned after at least eight months. They can be found in very specific places in the intestine, particularly in close contact with nerve cells and blood vessels."

What is more, the small group of long-lived macrophages play a very important role in the gastrointestinal tract, adds PhD student Sebastiaan De Schepper. "If the long-lived macrophages don't do their job properly, already after a few days the mice suffer from digestive problems. This leads to constipation or even the complete degeneration of the nervous system in the stomach and intestine." The discovery that long-lived macrophages do indeed exist in the intestine and that they are crucial for the normal functioning of the intestine is, therefore, immensely important.

These new insights offer promising opportunities for further research, concludes Boeckxstaens: "Next, we want to study the role of long-lived macrophages in human diseases where nerve cells of the intestine are affected, for instance in obese and diabetic patients with abnormal gastro-intestinal function. Moreover, the results can also be meaningful for brain research. In the brain, we have microglia, similar long-lived macrophages that play an important role in neurological conditions such as Alzheimer's and Parkinson's disease. Scientists currently believe that nerve cells in these patients die off because microglia do not provide sufficient care. Maybe one day research of the intestine can offer us a better understanding of these brain conditions."



9  Tutkimus / Tutkimus / Simvastatiinin kliiniset kokeet MS:n hoidossa
 Pvm: 18.05.2019 - 22:40:53 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Statins' potential to treat MS unrelated to lowering cholesterol

https://www.sciencedaily.com/releases/2019/05/190510095059.htm

May 10, 2019
The widely prescribed statin, simvastatin, can medically help patients with secondary progressive Multiple Sclerosis (SPMS) -- for reasons that might be unrelated to the drug's intended cholesterol lowering affects, a UCL study has found.

"Although this study cannot provide a final answer as to what exactly is the reason for the success of statins in progressive MS, it directs future researchers toward certain pathways," said lead author, Dr Arman Eshaghi (UCL Queen Square Institute of Neurology).

"This paves the way to find better drug targets for an incurable disease such as MS."

MS affects over 100,000 people in the UK, and most expect to develop a progressive form of the condition. It causes problems with how people walk, move, see, think, and feel. There is currently no cure for MS and little effective treatment for SPMS.

Primary research

Researchers used data from the UCL-led Phase 2 MS-STAT trial, which saw 140 people with SPMS either take a high dose of simvastatin (80mg a day) or a placebo for two years. Participants were aged 18-65 and had Expanded Disability Status Scale (EDSS) scores of between 4 and 6.5.

Throughout the trial, brain volume was assessed using MRI brain scans, levels of disability were assessed using the EDSS and serum cholesterol levels were measured, and participants completed several questionnaires that examined the impact of MS on their daily lives.

In the group taking simvastatin, brain volume loss was 43% less compared to those taking placebo. Smaller but still significant effects on two of the disability measures were also found, there was a slower change in EDSS (disability levels) and improved scores on a questionnaire which measures the impact of MS on daily life.

While this study showed simvastatin had a positive effect on delaying disability worsening and slowing brain atrophy (shrinkage) of people with SPMS, it was not entirely certain what the cause of that benefit was.

Latest study using computational models

In this study, published in Proceedings of the National Academy of Sciences (PNAS), researchers reanalysed the MS-STAT trial data and modelled hypothesised causal associations by which simvastatin leads to changes in brain atrophy, clinical and cognitive outcome measures, either directly or indirectly via changes in a patient's peripheral cholesterol level.

The study tested the hypothesis that the reduction in cholesterol levels was the cause of the positive impact simvastatin had on brain atrophy and on disability, against the alternative hypothesis that simvastatin effects were independent of peripheral cholesterol level.

Two computational models were developed. The first was a cholesterol-mediated model, in which the effects of simvastatin on clinical measures (both physical and cognitive) and brain atrophy are brought about by changes in cholesterol. The second was a cholesterol-independent model, in which simvastatin has a direct effect on the clinical and MRI outcome measures, independent of its effect on serum cholesterol levels.

Researchers tested both models using statistical analyses designed to answer causal questions, such as, is the reason that simvastatin helps reduce brain shrinkage the same as the reason it reduces cholesterol in the blood?

Results showed that simvastatin's effect on clinical outcomes and brain atrophy were largely independent of cholesterol.

Dr Eshaghi said: "Statins are naturally occurring, produced by some fungi, meaning that unlike most drugs that are designed for specific targets, they have (still after two decades of use in heart diseases) several unknown effects, and that is why this study is so important.

"My study tells us that statins help patients with MS for reasons different from how they help people lower their cholesterol. For example, statins can modulate other elements that are produced in the pathways before cholesterol, but have indirect effects on immune system."

Simvastatin is currently widely used to treat high cholesterol, and can be taken daily as an oral tablet. Statins have been shown to have an effect on the nervous system in protecting the nerves, and can also act as an anti-inflammatory treatment.

Professor Alan Thompson, Dean of the UCL Faculty of Brain Sciences and Chair of the Scientific Steering Committee of the Progressive MS Alliance, said: "Finding new and effective treatments for progressive MS is one of the key challenges facing the MS community and further advances will require a better understanding of underlying mechanisms.

"This study provides interesting and important insights into such mechanisms."

This study was carried out with researchers from the University of Cambridge and Imperial College London and was funded by National Institute for Health Research Biomedical Research Centre, The Engineering and Physical Sciences Research Council (EPSRC), the European Union's Horizon 2020 Research and Innovation Programme, Medical Research Council, and Wellcome Trust.

Phase 3 trial

In September last year the biggest ever trial SPMS in the UK was launched, led by Professor Jeremy Chataway (UCL Queen Square Institute of Neurology and National Hospital for Neurology and Neurosurgery).

With around 30 sites across the UK and Ireland, the MS-STAT2 trial involves 1,180 people with SPMS. Over 400 participants are currently in trial.

Co-funded by the MS Society, MS-STAT2 is the final stage trial of the drug treatment simvastatin for SPMS. This Phase 3 study will confirm whether simvastatin could become amongst the first drugs to slow or stop disability progression for this form of the condition, offering new hope to thousands.
*********
https://clinicaltrials.gov/ct2/show/NCT03387670
lTämän kliinisen kokeen tuloksia voi odotella elokuussa 2023.


"Simvastatin is one of the most promising treatment prospects for secondary progressive MS in our lifetime. People with this form of the condition have been waiting decades for a drug that works, which is why there's such excitement around being able to start the trial," said Professor Chataway, who is leading the trial and is a co-author on the PNAS paper.

"While it's still early days, we believe simvastatin could change lives."



10  Tutkimus / Tutkimus / Re: Suolistobakteerit, myeliini ja aivotoiminta
 Pvm: 18.05.2019 - 22:22:25 
Keskustelun aloitti HopeSprings | Kirjoittaja HopeSprings  
Link Between Gut Flora and Multiple Sclerosis Discovered

https://neurosciencenews.com/multiple-sclerosis-gut-flora-10003/

New findings made by the research group of Mireia Sospedra and Roland Martin from the University of Zurich’s Clinical Research Priority Program Multiple Sclerosis now suggest that it is worth broadening the research perspective to gain a better understanding of the pathological processes.

Inflammatory cascade

In the journal Science Translational Medicine, the scientists report that T cells – i.e. the immune cells responsible for pathological processes – react to a protein called GDP-L-fucose synthase. This enzyme is formed in human cells as well as in bacteria frequently found in the gastrointestinal flora of patients suffering from multiple sclerosis. “We believe that the immune cells are activated in the intestine and then migrate to the brain, where they cause an inflammatory cascade when they come across the human variant of their target antigen,” says Mireia Sospedra.

For the genetically defined subgroup of MS patients examined by the researchers, results show that gut microbiota could play a far greater role in the pathogenesis of the disease than previously assumed. Mireia Sospedra hopes that these findings can soon also be translated into therapy; she plans to test the immunoactive components of GDP-L-fucose synthase using an approach that the researchers have been pursuing for several years already.

Re-educating the immune system

“Our clinical approach specifically targets the pathological autoreactive immune cells,” says Sospedra. This approach therefore differs radically from other treatments that are currently available, which throttle the whole immune system. While these treatments often succeed in stopping the progression of the disease, they also weaken the immune system – and can thus cause severe side effects.

The clinical approach of the research group involves drawing blood from MS patients in a clinical trial and then attaching the immunoactive protein fragments onto the surface of red blood cells in a laboratory. When the blood is reintroduced into the bloodstream of patients, the fragments help to “re-educate” their immune system and make it “tolerate” its own brain tissue. This therapeutic approach aims for effective targeted treatment without severe side effects.