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Krooniset bakteeri-infektiot (Luettu 242328 kertaa)
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Re: Krooniset bakteeri-infektiot
Vastaus #360 - 06.07.2019 - 00:57:21
 
EBV infection and MS risk genes work together to facilitate MS

https://msra.org.au/news/ebv-infection-and-ms-risk-genes/

22 May, 2019

   Infection with Epstein-Barr Virus (EBV) is one of the known risk factors of developing MS but how EBV relates to MS risk is still an open question.
   New research by Australian researchers has looked at the effect of EBV infection on genetic activity in immune cells.
   Findings showed that EBV controls some MS risk genes.

What is Epstein Barr Virus (EBV)?

EBV (the virus that causes glandular fever) is a virus that belongs to the herpes virus family and it infects a type of immune cell in the blood known as a B cell. Once a person has been infected with EBV they carry the virus in their B cells for life, meaning their body has to continually control the EBV infection for the rest of their lifetime.

What do we already know about the link between EBV and MS?

Infection with EBV has long been known to be associated with the development of MS. However, while the majority of the population has been infected with the virus (only a small percent will develop recognisable symptoms), 100% of those with MS are thought to be infected.

This shows that while EBV plays a huge role in MS an EBV infection is not sufficient by itself to cause MS. So why do some people who contract EBV develop MS yet others never do? Part of the answer may lie in our genetics.

Previous research funded by MS Research Australia by Professor Michael Pender has shown that people with MS inadequately control these EBV hijacked immune cells and now Australian scientists might have uncovered an interesting interplay between the MS genetic risk factors and EBV.

A new link discovered between EBV and MS risk genes

In a new study, researchers at the Westmead Institute of Medical Research have investigated the way that EBV infection changes which genes the B cells are using and hence changes the way these cells act. Published in Genome Medicine, the researchers compared the gene activity of B cells that were infected with EBV and grown in the laboratory, and cells that had not been infected. They were particularly interested to see whether there would be any changes in the 200+ genetic elements that have already been identified as risk factors for the development of MS.

The research findings explained…

The research showed that a significant proportion of these MS risk genes were influenced by the presence of EBV. This means that:

  The infected cells used the MS risk genes differently in the presence of EBV.
   Some of these genes, in turn, controlled other genes in the cell, meaning there was a domino effect resulting in a number of changes within the cell.

   Further experiments showed that EBV may drive some of these changes at a cellular level through the binding of a molecule called EBNA2. When EBV is hijacking a cell it might try and use a number of cellular genes, and a portion of those are already known as MS risk genes.

This study indicates that the MS risk genes may be working together with EBV infection to facilitate the development of MS and that this interaction may be one way genetic changes act at a biological level to increase the risk of MS.

What do these new findings mean for the future?

A better understanding of the way that EBV infection relates to MS development is important to drive new therapeutic approaches for this disease. Professor Michael Pender’s work has led to the development of a new treatment strategy, currently in clinical trials, based on the idea that boosting a person with MS’s ability to control ongoing EBV infection could help treat MS.
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Re: Krooniset bakteeri-infektiot
Vastaus #361 - 15.07.2019 - 00:53:50
 
Are the 'viral' agents of MS, ALS and schizophrenia buried in our genome?

https://www.sciencedaily.com/releases/2019/07/190711141413.htm

July 11, 2019

What if the missing 'environmental' factor in some of our deadliest neurological diseases were really written in our genome?

Writing in Frontiers in Genetics, researchers from the University of Dusseldorf explain how viruses ended up in our DNA -- and what puts them in the frame in unsolved diseases like multiple sclerosis.

The enemy within

A whopping 8% of our DNA comes from viruses. Specifically, ones called retroviruses -- not because they're old, but because they reverse the normal process of reading DNA to write themselves into their host's genome.

Retroviruses are old though: they began merging with our earliest, primordial ancestors millions of years ago. Over the millennia, most of their remnants in our DNA -- known as human endogenous retroviruses or HERVs -- have been silenced by mutations. Others, which had evolved to fend off rival viruses, formed the prototypical immune system and to this day protect us from infection.

However, HERVs might also be the missing causative link in major 'unsolved' neurological diseases.

"HERVs have been implicated in the onset and progression of multiple sclerosis [MS], amyotrophic lateral sclerosis [ALS] and schizophrenia [SCZ]," says senior author Prof. Patrick Kuery. "Dormant HERVs can be reactivated by environmental factors such as inflammation, mutations, drugs, or infection with other viruses, so could provide a mechanism for their well-established epidemiological link to these disorders."

Role in MS

So far, the strongest evidence links HERVs to MS.

"MS is caused by direct autoimmune attacks on myelin -- the fatty coating of nerve cells -- in the brain and spinal cord," explains Kuery. "But we don't yet understand how these attacks are triggered."

A variety of studies suggest that reactivation of HERV could be just such a trigger.

"Retroviruses were first associated with MS in 1989, but only decades later was it realized that these are in fact HERVs.

"Subsequently, it was shown that levels of HERV RNA and protein -- the 'readouts' from reactivated HERV DNA -- are increased in the brain and spinal cord fluid [CSF] of sufferers, as well as in their brain tissue postmortem.

"Linking this HERV reactivation to autoimmune attacks in MS, it was found that HERV proteins can trigger an immune response against myelin, which triggers MS-like disease in mouse models."

Mechanistically, HERV proteins could trigger autoimmunity through 'molecular mimicry'.

"In addition to direct effects of HERV on myelinating cells, several groups report structural similarities between HERV and myelin oligodendrocyte glycoprotein -- a molecule displayed on the surface of myelin. This similarity could fool the immune system into damaging myelin, when it mounts an attack on HERVs."

Experimental proof in humans

Similar experiments have linked HERVs to the peripheral demyelinating disease CIDP, as well as more distinct disease processes like progressive loss of motor neurons in ALS (Lou Gehrig's disease).

In schizophrenia, a complex neurodevelopmental disorder, the link to HERVs is more circumstantial.

"HERV proteins have been reported to increase expression of schizophrenia-linked genes in cultured human brain cells," reports Kuery. "However, studies on schizophrenia sufferers show inconsistent changes in HERV expression in blood, CSF and postmortem brain tissue compared to healthy controls."

Whether or not HERVs contribute to these and other unexplained neurological conditions requires further investigation. An important step will be to test the effects of HERV-neutralizing antibodies in humans.

"Of note, in relapsing MS patients a phase 2b clinical trial using HERV protein-neutralizing antibody Temelimab has been conducted. We're now waiting to see if the treatment showed beneficial effects on remyelination or attenuated neurodegeneration," Kuery concludes.
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Re: Krooniset bakteeri-infektiot
Vastaus #362 - 15.07.2019 - 01:01:10
 
Epstein-Barr Virus and miRNAs: Partners in Crime in the Pathogenesis of Multiple Sclerosis?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456696/

2019 Apr 3

Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that modulate gene expression post transcriptionally. In healthy individuals, miRNAs contribute to maintaining gene expression homeostasis. However, the level of miRNAs expressed is markedly altered in different diseases, including multiple sclerosis (MS). The impact of such changes is being investigated, and thought to shape the immune system into the inflammatory autoimmune phenotype. Much is yet to be learned about the contribution of miRNAs in the molecular pathology of MS. Epstein-Barr virus (EBV) infection is a major risk factor for the development of MS. EBV encodes more than 40 miRNAs, most of which have been studied in the context of EBV associated cancers. These viral miRNAs regulate genes involved in cell apoptosis, antigen presentation and recognition, as well as B cell transformation. If EBV infection contributes to the pathology of MS, it is plausible that EBV miRNAs may be involved. Unfortunately, there are limited studies addressing how EBV miRNAs are involved in the pathogenesis of MS. This review summarizes what has been reported regarding cellular and viral miRNA profiles in MS and proposes possible interactions between the two in the development of MS.

***********
Conclusion

Of the environmental factors, substantial amount of data indicates that EBV is directly or indirectly involved in the pathogenesis of MS. Moreover, cellular, exosomal, plasma and erythrocyte miRNAs profiles indicate that these profiles are disrupted in MS patients, compared to healthy controls. Although a large number of studies have investigated the significance of EBV encoded miRNAs in altering the levels of viral and cellular genes in EBV associated malignancies, much less is known in the context of MS. On the one hand, the disrupted homeostasis of cellular miRNAs in MS appears to serve the ongoing inflammation linked to the disease, whilst on the other hand, they may aid in supporting the survival of EBV infected cells by positively influencing viral miRNAs that function in evading anti-EBV immune response. Dysregulated cellular miRNAs may also pave the way for CNS infiltration by inflammatory cells and EBV infected cells. It is reasonable to think that EBV miRNAs in MS CNS can also impact CNS resident cells, particularly those involved with MS pathology. Thus, investigating the targets and role of EBV miRNAs in MS, mainly in peripheral blood, CSF, brain, and CNS draining lymph nodes, could shed light on disease mechanism not yet explored.



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Re: Krooniset bakteeri-infektiot
Vastaus #363 - 02.08.2019 - 00:31:19
 

Neuronal loss or dysfunction in patients with early Lyme neuroborreliosis: a proton magnetic resonance spectroscopy study of the brain.


https://europepmc.org/abstract/med/31076877

10 May 2019

Abstract
BACKGROUND:We hypothesized that since Borrelia burgdorferi causes systemic inflammation and infects the brain, it may lead to alterations in cerebral metabolism, as measured by 1H-magnetic resonance spectroscopy (1H-MRS). The purpose of our study was to determine whether 1H-MRS could detect brain metabolite alterations in patients with early Lyme neuroborreliosis (LNB) in normal-appearing brain tissue on the conventional magnetic resonance imaging (MRI).

METHODS:Twenty-six patients diagnosed with early LNB and twenty-six healthy volunteers as a control group have been involved in the study. All of them underwent routine MRI protocol using 3.0-T MRI scanner. 1H-MRS examinations were performed with repetition time (TR) = 2000 ms, and echo time (TE) = 135 ms. Single voxels were positioned in the anterior and posterior parts of the right and left frontal lobes.

RESULTS:We found a statistically significant decrease of the N-acetylaspartate/creatine ratio within the anterior part of the right and left frontal lobes (p ≤ 0.001 and p = 0.001 respectively) and in the posterior part of the right and left frontal lobes (p ≤ 0.001 and 0.031) in the patients with LNB.

CONCLUSION:A significant reduction in NAA/Cr ratio in comparison with the controls suggests the presence of diffuse neuronal loss in patients with early LNB.

******
Tutkimus koski alkuvaiheesa olevaa borrelioosia. Mutta myöhemmässä vaiheessa jos on plakkeja aivoissa? Syy voi olla MS-taudin tai borrelioosin. Vain asiantunteva radiologi pystyy erottamaan kumpi on kumpi. Näin minulle kertoi neurologi, joskaan ei Suomessa.

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Re: Krooniset bakteeri-infektiot
Vastaus #364 - 13.08.2019 - 00:10:19
 
How do ancient viruses cause MS and other neurological diseases?

https://www.medicalnewstoday.com/articles/325718.php?type=medical-news

Ancient viruses have left behind traces in our DNA. Researchers believe these contribute to neurological conditions. Could inhibiting our viral passengers pave the way for future treatments?

Ancient viruses link to neurological conditions
What links neurological conditions and ancient viruses?

Transposable elements, which scientists also call transposons or jumping genes, are stretches of DNA that harbor the ability to move around our genome.

Scientists can trace back one type of transposon — human endogenous retroviruses (HERVs) — to ancient retroviruses that inserted themselves into the human genome millions of years ago. HERVs make up about 8% of our DNA.

Some HERVs hold crucial functions during processes such as embryonic development. But most HERVs lie dormant, silenced by DNA modifications.

Yet, in a recent review article in Frontiers in Genetics, researchers from Heinrich Heine University in Dusseldorf, Germany, detail how some HERVs may be reactivated and wreak havoc in our brain and central nervous system.

HERVs in neurological diseases

Back in 1989, Hervé Perron, then at the University of Grenoble in France, was the first to identify the presence of viral particles in cell cultures isolated from the cerebrospinal fluid (CSF) of a person with multiple sclerosis (MS). He later discovered that these originated from a transposon called HERV-W.

Activation of this dormant HERV results in an immune reaction. HERV-W envelope (ENV) RNA and protein are present at increasing levels in the serum and CFS of people with MS, but only rarely in those without the condition.

"Linking this HERV reactivation to autoimmune attacks in MS, it was found that HERV proteins can trigger an immune response against myelin, which triggers MS-like disease in mouse models," explains Patrick Kuery, a professor of neurodegeneration and senior review author.

Several triggers can reactivate HERVs. One of them is infection with common viruses, such as the Epstein-Barr virus that causes infectious mononucleosis, and other members of the herpes virus family.

How childhood viral infections may later drive multiple sclerosis

Viral infections during childhood leave lasting marks in the brains of people with MS.
Research also suggests that immune system mediators and environmental factors, such as diet and drugs, can switch HERVs back on, although there is limited evidence at this point.

MS is not the only neurological disease where scientists suspect HERV involvement. A number of studies have implicated reactivation of HERV-K in amyotrophic lateral sclerosis (ALS), a form of motor neuron disease.

When it comes to schizophrenia, the case is less clear.

"HERV proteins have been reported to increase expression of schizophrenia-linked genes in cultured human brain cells," explains Kuery. "However, studies on schizophrenia [patients] show inconsistent changes in HERV expression in blood, CSF, and postmortem brain tissue compared to healthy controls."

Can deactivating HERV improve MS?

In MS, the immune system attacks myelin, the protective layer that coats many neurons in the central nervous system.

Repairing this myelin damage by allowing the cells in the CNS to remyelinate neurons may prove an effective strategy to treat MS.

Since identifying HERV-W in MS patients, Perron co-founded the pharmaceutical company GeNeuro and developed a monoclonal antibody called GNbAC1 that targets the HERV-W ENV protein. Scientists are currently testing the antibody in clinical trials.

In a recent paper published in Proceedings of the National Academy of Sciences of the United States, Kuery, Perron, and colleagues dug deeper into the mechanism that links HERV-W to MS.

The team found cells that contained the HERV-W ENV protein in close proximity to neurons in brain tissue of MS patients, particularly in areas that contained chronic and acute MS lesions.

Dr. Tobias Derfuss, a professor in clinical neuroimmunology at the University of Basel in Switzerland, was a principal investigator of one of the clinical trials investigating the use of GNbAC1 in MS and a member of the steering committee for a further trial.

Writing in Therapeutic Advances in Neurological Disorders, Dr. Derfuss comments: "This treatment approach of GNbAC1 and the concept of a HERV-associated pathophysiology in MS remain controversial."

He explains that the results of the clinical trials investigating GNbAC1 for the treatment of MS indicate that the antibody does not prevent the immune system from attacking myelin, meaning it does not prevent MS.

The antibody may, on the other hand, kickstart remyelination.

   "Pharmacodynamic and imaging data do not reveal any immunomodulatory effects of GNbAC1. MRI changes during a phase IIb study with GNbAC1 are compatible with remyelination."

MS is a complex disease, and scientists do not fully understand the biology of HERVs. A HERV-modifying therapeutic may prove to be a promising treatment for people living with MS, but its true potential remains to be seen.
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Re: Krooniset bakteeri-infektiot
Vastaus #365 - 20.09.2019 - 13:50:01
 

Preliminary safety and efficacy of ATA188, a pre-manufactured, unrelated donor (off-the-shelf, allogeneic) Epstein-Barr virus-targeted T-cell immunotherapy for patients with progressive forms of multiple sclerosis


https://onlinelibrary.ectrims-congress.eu/ectrims/2019/stockholm/278696/michael.
pender.preliminary.safety.and.efficacy.of.ata188.a.pre-manufactured.html?f=listi
ng%3D0%2Abrowseby%3D8%2Asortby%3D1%2Asearch%3Dbar-or


Introduction: Evidence suggests Epstein-Barr virus (EBV) infection is associated with multiple sclerosis pathogenesis. In patients (pt) with progressive forms of MS (pMS), autologous EBV-specific T cells may prevent progression and improve symptoms (Pender, et al. JCI Insight. 2018).

Objectives: To evaluate ATA188, an off-the-shelf, allogeneic, EBV-targeted T cell immunotherapy comprised of HLA-matched, in vitro-expanded, cytotoxic T lymphocytes in a first-in-human, multicenter, 2-part study in adults with pMS (NCT03283826). Preliminary data are reported.

Methods: Eligible pt (age 18‒< 66) are EBV-seropositive with pMS and an Expanded Disability Status Scale (EDSS) score of 3‒7. Cohorts (cht) 1‒4 (6‒9 pt/cht) receive escalating doses of ATA188.
1° endpoints: safety and identification of the recommended phase 2 dose (RP2D) of ATA188. Efficacy criteria: EDSS, MS Impact Scale-29, Fatigue Severity Scale, and 12-Item MS Walking Scale scores; timed 25-foot walk; 9-hole Peg Test; and visual acuity. A responder (R) has sustained ≥ minimal clinically significant (MCS) improvement from BL in 2 consecutive evaluations on ≥2 efficacy criteria; a partial responder (PR) has ≥ MCS improvement from baseline (BL) in any 1 evaluation on ≥2 efficacy criteria; and a non-responder (NR) has ≥ MCS decline from BL in any 1 evaluation on ≥2 efficacy criteria (if both criteria are met, pt is NR). Plasma inflammatory biomarkers (IL-2, IL-1β, TNF-α, IL-6) are monitored throughout treatment.

Results: As of 27 May 2019, 19 pt (53% male; median age, 56 years) have enrolled (6 in each of cht 1‒3; 1 in cht 4) and received ≥1 dose of ATA188. Treatment-emergent AEs (TEAE) occurred in 63% (12/19) pt and treatment-related AEs (TRAE) in 37% (7/19) pt; 1 pt (cht 2) had a grade ≥ 3 TEAE, and 1 (cht 4) had a serious TRAE. No dose-limiting toxicities or fatal TEAE have been reported. Efficacy data are available for cht 1 and 2: cht 1, 1 R, 1 PR, and 4 NR at 6 months and 1 R, 0 PR, and 1 NR at 12 months; cht 2, 2 R, 4 PR, and 0 NR at 6 months. On measures of disability, 3/6 showed improvement and 3/6 showed decline in cht 1; 4/6 showed improvement and 1/6 showed decline in cht 2. Inflammatory cytokines remained at or near baseline.

Conclusion: Preliminary data indicate ATA188 is well tolerated and improves efficacy measures in adults with pMS, even at lower doses. These results support continuing part 1 to identify RP2D for part 2, (randomized, double-blind, placebo-controlled portion).
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Re: Krooniset bakteeri-infektiot
Vastaus #366 - 20.09.2019 - 13:56:30
 
Sama, mutta ymmärrettävässä muodossa. Ja tämä on siis ATA188 tutkimusta:


Epstein-Barr virus–specific T cell therapy for progressive multiple sclerosis


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302936/

Abstract

BACKGROUND. Increasing evidence indicates a role for EBV in the pathogenesis of multiple sclerosis (MS). EBV-infected autoreactive B cells might accumulate in the CNS because of defective cytotoxic CD8+ T cell immunity. We sought to determine the feasibility and safety of treating progressive MS patients with autologous EBV-specific T cell therapy.

METHODS. An open-label phase I trial was designed to treat 5 patients with secondary progressive MS and 5 patients with primary progressive MS with 4 escalating doses of in vitro–expanded autologous EBV-specific T cells targeting EBV nuclear antigen 1, latent membrane protein 1 (LMP1), and LMP2A. Following adoptive immunotherapy, we monitored the patients for safety and clinical responses.

RESULTS. Of the 13 recruited participants, 10 received the full course of T cell therapy. There were no serious adverse events. Seven patients showed improvement, with 6 experiencing both symptomatic and objective neurological improvement, together with a reduction in fatigue, improved quality of life, and, in 3 patients, reduced intrathecal IgG production. All 6 patients receiving T cells with strong EBV reactivity showed clinical improvement, whereas only 1 of the 4 patients receiving T cells with weak EBV reactivity showed improvement (P = 0.033, Fisher’s exact test).

CONCLUSION. EBV-specific adoptive T cell therapy was well tolerated. Clinical improvement following treatment was associated with the potency of EBV-specific reactivity of the administered T cells. Further clinical trials are warranted to determine the efficacy of EBV-specific T cell therapy in MS.

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Re: Krooniset bakteeri-infektiot
Vastaus #367 - 29.09.2019 - 16:15:21
 
Genomic map implicates broad immune cell involvement in multiple sclerosis

https://www.sciencedaily.com/releases/2019/09/190926141655.htm

September 26, 2019
The International Multiple Sclerosis Genetic Consortium (IMSGC) reports the results of its latest study, "Multiple sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility," in the journal Science today: the highly productive collaborative group presents a new milestone in its efforts to understand the genetic basis of multiple sclerosis (MS). In a study of 115,803 individuals, the authors have identified 233 sites or loci in the human genome that contribute to the onset of MS. This is the largest study to date in MS and is based on the generous contribution of genetic material from 47,429 MS patients and 68,374 healthy individuals. The study's results confirm earlier results and offer a rich new perspective on the molecular events that lead some individuals to develop MS: it appears that dysfunction of many different immune cell types, both in the peripheral blood and the brain, contribute to triggering a cascade of events that ultimately leads to brain inflammation and neurodegeneration.

Dr. Philip De Jager, who directs the Multiple Sclerosis Center and the Center for Translational & Computational Neuroimmunology at Columbia University Irving Medical Center in New York City, and the principal investigator of the study says that "the study has created a detailed genetic map of MS, identifying over two hundred regions of the human genome that influence a large number of different immune cells, highlighting the fact that this disease is not caused by a single immune cell type but rather by a broad dysfunction of the immune system." MS has an initial inflammatory component and a secondary neurodegenerative component, so the investigative team looked closely at available data from human brain to assess whether changes in brain cells contribute to the onset of MS. Until now, it appeared that immune cells found in blood that come from the bone marrow played a critical role; the new study confirms this but also implicates microglia, the immune cells that live in the human brain. However, there is little evidence that other brain cells such as neurons that carry electrical signals in the brain are implicated in triggering MS.

Dr. Nikolaos Patsopoulos, Director of Systems Biology and Computational Science Program at the Ann Romney Center for Neurologic Diseases of Brigham & Women's Hospital and Harvard Medical School in Boston, says that "our study explains approximately half of the heritability of MS, establishing MS as one of the well-characterized common diseases in terms of their genetic architecture." He adds that "this study highlights the complexity of the genetic contribution to MS susceptibility by identifying several regions of the genome with multiple genetic variants that play a small role. Further, we report the first ever association of genetic variant in chromosome X with MS, a disease that affects mainly young women. This study more than doubled our knowledge of MS genetics, however our findings suggest that there is more work to be done to fully understand how the human genome is involved in MS."

Dr. Tomas Olson, an author on the study from the Karolinska Institute in Stockholm, Sweden says that "this collaborative effort integrated multiple streams of North American and European funding to establish an important foundation for future projects that will uncover the sequence of events leading from health to MS. These genetic variants are not sufficient to cause MS; they interact with a host of environmental factors, making it more likely that a viral infection or other exposure triggers an autoimmune reaction against the brain and spinal cord."

Dr. Adrian Ivinson, Chief Operating Officer of the UK Dementia Research Institute who is also an author of this study adds that "this study reflects the combined, collaborative efforts of the international MS Genetics community to advance our understanding of MS disease mechanisms and the continuing support of the National MS Society in the completion of this project, the development of young investigators and support for basic research in MS. It is an excellent example for the success of collaborative team-oriented science in medicine."

This study is an important milestone in identifying which genetic variants play a role in triggering MS, but it unfortunately does not clarify why some MS patients have a more severe course than others. The IMSGC is pursuing that question in other projects. The results of this project will impact most the development of clinical algorithms to manage individuals at risk of developing MS and the development of treatments for preventing MS. All current treatments aim to stop the inflammation after it has already started, so the study of MS genetics has opened a unique perspective on the earliest events that lead to the disease and that can now be targeted by drug-development efforts.

The Columbia University Multiple Sclerosis Center provides compassionate care for MS patients, and we engage with our our patients to perform both basic research that brings new insights into our understanding of the disease and clinical research that brings the latest technologies and medications with which to improve our management of each patient. This is study is an example of Columbia's leadership of international collaborations in the field of MS and of the emerging foundation for Precision Medicine in MS.

******
Geenit eivät aiheuta MS:ää vaan ympäristö ja virukset. No, tulipahan sekin nyt varmistettua.
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