Cystic fibrosis, Multiple sclerosis, Muscular dysrophy, etc.

waltky

Wise ol' monkey
Feb 6, 2011
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Okolona, KY
Wonder if it'll work against multiple sclerosis?...
:confused:
Researchers Override a Disease-Causing Gene Mutation
June 15, 2011 : Scientists report they have found a new way to change the genetic code within living cells, a discovery that could lead to effective treatments for inherited diseases caused by a common genetic mutation.
Researchers at the University of Rochester in New York studied a specific mutation in the human genetic code called a "premature stop codon" that is common to a number of diseases, including cystic fibrosis and muscular dystrophy. It is estimated that up to one-third of inherited disorders are caused by this defective piece of code. The genetic code is a set of instructions in a gene that tells a cell how to make specific proteins, chemicals that are key to an organism's normal development and function. The premature stop codon, which scientists liken to a red stop light, is a mutation that orders cells to stop reading essential genetic instructions part-way through protein synthesis, resulting in an incomplete or shortened protein and potentially serious health consequences.

John Karijolich is the study’s lead author. “So what will happen when you have a [shortened] protein, you end up losing whole sections of the protein and whole parts of the protein that are engaged in reactions. So it would be the lack of those domains of the protein that results in disease," he said. Researchers altered messenger RNA, or mRNA, the chemical which conveys the genetic instructions from DNA, so that the stop signal codon was changed, in effect, to a green light or “go” signal, producing normal, full-length protein strands. The scientists demonstrated the work in the test tube and in laboratory yeast.

Investigators created another type of RNA, called guide RNA, to target and fix stop-codons in regular RNA. Karijolich hopes that one day RNA therapy can be administered to people with diseases like muscular dystrophy. “It would have to be once the patient is diagnosed and it then would be like a form of treatment. It wouldn’t be a cure. It would have to be continual. If it was possible you would have to continually take this RNA supplement that would continue to direct the modification of this RNA stop-codon," he said. An article on RNA repair is published in the journal Nature.

Source
 
Wonder if it'll work against multiple sclerosis?...
:confused:
Researchers Override a Disease-Causing Gene Mutation
June 15, 2011 : Scientists report they have found a new way to change the genetic code within living cells, a discovery that could lead to effective treatments for inherited diseases caused by a common genetic mutation.
Researchers at the University of Rochester in New York studied a specific mutation in the human genetic code called a "premature stop codon" that is common to a number of diseases, including cystic fibrosis and muscular dystrophy. It is estimated that up to one-third of inherited disorders are caused by this defective piece of code. The genetic code is a set of instructions in a gene that tells a cell how to make specific proteins, chemicals that are key to an organism's normal development and function. The premature stop codon, which scientists liken to a red stop light, is a mutation that orders cells to stop reading essential genetic instructions part-way through protein synthesis, resulting in an incomplete or shortened protein and potentially serious health consequences.

John Karijolich is the study’s lead author. “So what will happen when you have a [shortened] protein, you end up losing whole sections of the protein and whole parts of the protein that are engaged in reactions. So it would be the lack of those domains of the protein that results in disease," he said. Researchers altered messenger RNA, or mRNA, the chemical which conveys the genetic instructions from DNA, so that the stop signal codon was changed, in effect, to a green light or “go” signal, producing normal, full-length protein strands. The scientists demonstrated the work in the test tube and in laboratory yeast.

Investigators created another type of RNA, called guide RNA, to target and fix stop-codons in regular RNA. Karijolich hopes that one day RNA therapy can be administered to people with diseases like muscular dystrophy. “It would have to be once the patient is diagnosed and it then would be like a form of treatment. It wouldn’t be a cure. It would have to be continual. If it was possible you would have to continually take this RNA supplement that would continue to direct the modification of this RNA stop-codon," he said. An article on RNA repair is published in the journal Nature.

Source

Fascinating.

Cystic Fibrosis is horrible. Hopefully this is a major advancement.
 
Multiple Sclerosis is defined as a disease which the nerves of central nevervous system, the brain and the spinal cord degenerates.the Myelin which provides a insulation or covering of the nerves,that improves the conduction of impulses together with the nerves and also it is important in maintaining the healthiness of the nerves. but in Multiple Sclerosis there is an inflammation that causes the myelin to disappear. As a result the electrical impulses that circulate along the the nerves slow downs. In addition in damages the nerves which will further affects the persons effectivity to perform task which controlled by the nervous system such as speech,vision,writing,walking and memory.
 
Could help asthma patients too...
:cool:
'Brush' offers clues to fighting lung disease
23 August 2012 - In people with cystic fibrosis, mucus is not properly cleared from the lungs
Scientists say the discovery of an internal "brush" that helps clear lungs of unwanted matter could help them understand more about lung diseases. A team from the University of North Carolina found that the brush-like layer pushes out sticky mucus and the foreign bodies it contains. Writing in Science, it says that could help identify what goes wrong in cystic fibrosis, asthma and similar diseases. UK lung experts said the work aided understanding of how lungs function. The mucus, which helps collect inhaled pollutants, emerges as a runny nose and a wet cough.

Until now, most experts believed a watery substance acted as a lubricant and helped separate mucus from the cells lining airways. But this did not tally with the fact that mucus remained in its own distinct layer. The researchers used imaging techniques to examine what was happening within the lungs. They were able to see a dense meshwork of human bronchial epithelial cell cultures. The brush-like layer consists of protective molecules that keep sticky mucus from reaching the cilia and epithelial cells, thus ensuring the normal flow of mucus.

'Flood' risk

Dr Michael Rubinstein, who led the study, said: "The air we breathe isn't exactly clean, and we take in many dangerous elements with every breath. "We need a mechanism to remove all the junk we breathe in, and the way it's done is with a very sticky gel, called mucus, that catches these particles and removes them with the help of tiny cilia." "The cilia are constantly beating, even while we sleep. "In a co-ordinated fashion, they push mucus, containing foreign objects, out of the lungs, and we either swallow it or spit it out. "These cilia even beat for a few hours after we die. If they stopped, we'd be flooded with mucus that provides a fertile breeding ground for bacteria." The team says the brush layer protects cells from the sticky mucus and acts as a "second barrier" in case viruses or bacteria penetrate the mucus.

But in conditions such as cystic fibrosis or chronic obstructive pulmonary disease (COPD), the "brush" fails to work properly, they suggest, becoming squashed and trapping mucus, which then becomes stuck to cells. Dr Rubenstein said: "The collapse of this brush is what can lead to immobile mucus and result in infection, inflammation and eventually the destruction of lung tissue and the loss of lung function." He said the findings should help inform new research into such lung conditions. Prof Stephen Spiro, vice-chairman of the British Lung Foundation, said: "Mucus has a complex biological make-up and forms a vital part of the lungs' defence mechanism against potentially harmful or irritating substances, which are inhaled as small particles. "Research such as this helps our understanding [of] how this system works, and of the complex mechanisms deep within our lungs which protect us from the atmosphere we breathe in."

BBC News - 'Brush' offers clues to fighting lung disease
 
Breathalyzer test for lung infections...
:cool:
Lung infection identified using 'breath-print'
10 January 2013 - Identifying the "smell" of different types of lung bacteria could lead to a simple breath test to diagnose infections, a study on mice, in the Journal of Breath Research, suggests.
Breath analysis could reduce lung infection diagnosis times from weeks to minutes, the Vermont researchers said. Scientists have already researched breath tests to diagnose asthma and cancer. An expert said breath analysis was "an important and emerging field". Diagnosing bacterial infections traditionally means collecting a sample that is used to grow bacteria in the lab. This bacteria is then tested to classify it and see how it responds to antibiotics, which can take time.

Doctors see breath analysis, in contrast, as a fast and non-invasive method of diagnosing diseases. For the study, researchers from the University of Vermont analysed volatile organic compounds (VOCs) given off in exhaled breath by different bacteria as well as different strains of the same bacterium. They infected mice with two bacteria that are both common in lung infections - Pseudomonas aeruginosa and Staphylococcus aureus - and sampled their breath after 24 hours.

'Useful tool'

The compounds in their breath were analysed using a technique called secondary electrospray ionisation mass spectrometry (SESI-MS), which is capable of detecting extremely small elements of the chemicals present in their breath. The researchers said they found a "statistically significant" difference between the breath profiles of the mice infected with the bacteria and the mice that were uninfected. They also said they were able to differentiate between two species of bacteria and two different strains of the same P. aeruginosa bacterium.

But Jane Hill, co-author of the study, from the University of Vermont College of Medicine, said there were still some challenges to overcome with "breath-prints". "We are now collaborating with colleagues to sample patients in order to demonstrate the strengths, as well as limitations, of breath analysis more comprehensively," she said. Richard Hubbard, professor of respiratory epidemiology at Nottingham City Hospital and a spokesman for the British Lung Foundation, said breath analysis was already being used to diagnose children with asthma. "Breath analysis is an emerging field and is likely to take off across the board. It could be a very useful tool for children with cystic fibrosis, for example, as a guide on how to treat them," he said.

BBC News - Lung infection identified using 'breath-print'
 
The infection has been on the rise over the past decade in patients...
:eusa_eh:
Cystic fibrosis bug 'can spread between patients'
30 March 2013 - A dangerous infection which is becoming more common in people with cystic fibrosis can spread between patients, UK researchers say in The Lancet.
Doctors previously thought the Mycobacterium abscessus bacteria could only be caught from water and soil. But hospitals around the world may now have to change the way patients are treated, the study says. Around 3-10% of cystic fibrosis patients in Europe and the US are infected with the hard-to-treat bug. There are around 9,000 people with cystic fibrosis in the UK although around one-in-25 people carries the faulty gene which causes the condition.

It affects the internal organs, especially the lungs and digestive system, by clogging them with thick sticky mucus which makes it hard to breathe and digest food. Researchers writing in The Lancet do not know exactly why Mycobacterium abscessus - which is distantly related to the bacteria that causes tuberculosis - is more likely to infect people with cystic fibrosis but it could be related to problems with the immune system.

It causes lung damage, and can be incredibly hard to treat with infected patients needing months of treatment with toxic drugs. Although the infection has been on the rise over the past decade, doctors always believed it could not spread between humans. But by looking at DNA from almost 170 samples of the bacterium, and using that to create a family tree, researchers found that it can indeed spread from person to person.

Infection control
 
Mebbe dey'll find a cure in the next 10 years...
:confused:
New lungs buy time but don't cure cystic fibrosis
13 June`13 WASHINGTON (AP) — The 10-year-old Pennsylvania girl who fought for a lung transplant has a difficult journey ahead. The transplant isn't a cure for her cystic fibrosis, and new lungs don't tend to last as long as other transplanted organs.
But it can extend life by years, buying some time. "You're keeping them alive and hopefully well, hoping that something else will come along that will make the big difference," said Dr. Anastassios Koumbourlis, pulmonary chief at Children's National Medical Center in the nation's capital. Sarah Murnaghan, who is recovering from Wednesday's operation at the Children's Hospital of Philadelphia, made headlines as her parents challenged national policy over how children under 12 are placed on the waiting list for donated lungs. Lost in the debate over how to give out scarce organs was this broader question: How well do children with cystic fibrosis fare when they do get a new set of lungs?

Fortunately, few children get sick enough anymore to need transplants, said Dr. Stuart Sweet, pediatric lung transplant chief at Washington University in St. Louis. Treatments for the genetic disease have improved so much over the past decade that patients live much longer before their lungs start to wear out. About 30,000 Americans live with cystic fibrosis, which causes sticky mucus to build up in the lungs, leading to life-threatening infections in the lungs and problems in other organs. Only a few decades ago, children with the disease seldom survived elementary school. Now the typical life expectancy is about 37 years and growing.

A 2007 study published in the New England Journal of Medicine prompted major controversy over whether lung transplants offered enough survival benefit to be used for cystic fibrosis. Ultimately, doctors decided it did, for the right patient who is out of options. Since then, about 150 to 200 people with the disease, mostly teens and adults, have gotten lung transplants every year, according to a patient registry run by the Cystic Fibrosis Foundation. Over 80 percent of patients who get new lungs survive a year, and over 50 percent are alive after five years, the registry shows.

That's a sobering statistic, although some people survive much longer. For comparison, well over 90 percent of people who receive a kidney transplant survive five years. "We expect it will be a long road, but we're not going for easy, we're going for possible," Sarah's family said in a statement after her surgery. Sweet said the issue isn't the cystic fibrosis but that lungs simply are difficult to transplant, no matter what the underlying disease. "The reality is that lung transplantation is not a perfect solution," Sweet said.

After all, "this is the only organ we transplant that's in contact with the outside world," added Dr. Karen McCoy, pulmonology chief at Nationwide Children's Hospital in Columbus, Ohio. For cystic fibrosis patients, the donated lungs don't contain the defective gene that caused their own lungs to clog — so they won't fill with mucus again. Cystic fibrosis will continue to damage their pancreas, intestines and other parts of the body, requiring ongoing treatment to deal with nutritional problems and other symptoms.

More New lungs buy time but don't cure cystic fibrosis
 
Stem cell transplants have helped some paralyzed patients to walk on their own...

Cancer treatment has 'remarkable' results against type of MS
Jan. 19, 2016 - Some paralyzed patients in a study have been able to walk on their own after being given stem cell transplants from their own bone marrow.
Multiple sclerosis patients given a form of treatment usually used with cancer patients -- which involves chemotherapy and a stem cell transplant -- have shown what doctors are calling "remarkable results." The aggressive treatment, autologous haematopoietic stem cell transplantation, or AHSCT, is generally used for blood and bone cancers, however researchers in England, Brazil, and the United States have been testing its effects on people with relapsing remitting multiple sclerosis in a small study.

RRMS is characterized by flare-ups of worsening neurologic function that fade either partially or completely. About 85 percent of people with multiple sclerosis are initially diagnosed with RRMS, according to the National MS Society, most of whom are diagnosed in their 20s and 30s. "The new treatment is showing some remarkable results in the small number of patients we have treated so far," said Basil Sharrack, a professor at Sheffield Teaching Hospital, in a press release. "It is important to stress however that this treatment is unfortunately not suitable for everyone."

Cancer-treatment-has-remarkable-results-against-type-of-MS.jpg

Although 85 percent of MS patients are initially diagnosed with RRMS, researchers caution that AHSCT may not help all MS patients.​

Multiple sclerosis causes the immune system to attack the lining of nerves in the brain and spinal cord, causing scar tissue to be formed, interrupting communication between nerves. The progressive condition is characterized by fatigue, numbness, problems with vision and balance, and gradually becomes worse to cause issues with walking and mobility, in addition to other related symptoms.

In the current study, and a previous study conducted at Northwestern University, RRMS patients were given chemotherapy to stop immune attacks on the body. Stem cells, which were harvested from patients' own blood or bone marrow before chemotherapy, are then transplanted back into the patients. "The immune system is being reset or rebooted back to a time point before it caused MS," said John Snowden, a researchers at Royal Hallamshire Hospital. The study was limited to RRMS patients who have had two or more relapses in the last year and have not been helped by other treatments over the course of at least 10 years. Researchers are still reviewing data and will continue to follow the patients for five years to track their progress.

http://www.upi.com/Health_News/2016...gainst-type-of-MS/5461453214395/?spt=slh&or=4
 
Loss of taste in MS patients...

Brain lesions may be cause of taste loss in MS patients
Feb. 8, 2016 -- Brain lesions caused by multiple sclerosis may damage the sense of taste in patients, researchers at the University of Pennsylvania found in a recent study.
Though they said a definite causal link between the two wasn't proven in the study, a much higher rate of patients had taste impediments than was expected, and the more lesions seen on an MRI, the worse the taste function of the patient. More common symptoms of MS include fatigue, cognitive difficulties, and vision loss. Taste problems are reported less often, researchers said, however many people mistake issues with smell and taste, so they may be under-reported. "It appears that a sizable number of these patients exhibit taste deficits, more so than originally thought," Dr. Richard Doty, a professor at the University of Pennsylvania and director of the Smell and Taste Center, said in a press release. "This suggests that altered taste function, though less noticeable than changes in vision, is a relatively common feature in MS."

For the study, published in the Journal of Neurology, researchers recruited 73 multiple sclerosis patients and 73 healthy people, giving them a standard taste test -- sweet, sour, bitter and salty -- and taking MRI scans of both groups for 52 regions of the brain affected by MS. Overall, twice as many MS patients' taste scores were deficient than was expected based on previous studies. The percentage of MS patients whose identification of taste score fell below the 5th percentile of healthy people was 15.07 percent for caffeine, 21.9 percent for citric acid, 24.66 percent for sucrose, and 31.50 for sodium chloride.

The researchers said the new association between smell and MS could help doctors better diagnose the disease and manage its symptoms. "These findings give us a better insight about that relationship, as well as the areas of the brain that are more likely to impact the dysfunction when scarred from the disease," Doty said.

Brain lesions may be cause of taste loss in MS patients

See also:

Cognitive behavioral therapy changes brain volume, study says
Feb. 5, 2016 - By studying the physiological effects of different therapies, researchers hope to improve mental health outcomes.
Patients with social anxiety disorder benefited from just nine weeks of cognitive behavioral therapy delivered via the Internet. According to a new study published in the journal Translational Psychiatry, the therapy not only reduced the anxiety levels of patients but physically altered their brains -- decreasing volume and activity in certain parts of the brain. The study was carried out by neuroscientists and psychiatrists from several Swedish universities and involved 26 participants diagnosed with social anxiety disorder, one of the most common mental health problems.

MRI scans before after nine weeks of CBT showed significant shrinkage of the amygdalae, a portion of the temporal lobes linked with memory, decision-making and emotional reactions. "The greater the improvement we saw in the patients, the smaller the size of their amygdalae," lead study author Kristoffer Mansson, a doctoral student at Linkoping University, explained in a news release. "The study also suggests that the reduction in volume drives the reduction in brain activity."

Cognitive-behavioral-therapy-changes-brain-volume-study-says.jpg

MRI scans showed that just nine weeks of cognitive behavioral therapy changed brain structure in patients with social anxiety disorder, a new study said​

Cognitive behavioral therapy is a type of psychotherapy focused on problem solving as opposed to analysis. Therapists aim to augment thought processes and their related behaviors in patients to diminish anxiety or depression symptoms.

Mansson and his research partners are studying the physiological effects of different therapies as a way to improve mental health outcomes. "Although we didn't look at that many patients, this work provides some important knowledge -- especially for all the sufferers," Mansson said. "Several studies have reported that certain areas of the brain differ between patients with and without anxiety disorders," he added. "We've shown that the patients can improve in nine weeks -- and that this leads to structural differences in their brains."

Cognitive behavioral therapy changes brain volume, study says
 
Canadian doctors come up with Radical Procedure to Treat MS...
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Radical Procedure to Treat MS Shows Great Promise
June 24, 2016 - Canadian researchers have succeeded in getting patients with an aggressive form of multiple sclerosis out of wheelchairs and moving again. The protocol is risky, even potentially deadly, but the outcomes have been astonishing and are being closely watched by other neurologists.
Multiple sclerosis is the leading crippler of young adults, with an estimated 2.3 million people around the world affected by the neurological disease. In those with MS, the immune system mistakenly attacks the fatty outer layer of brain neurons, called myelin, a situation that over time that can lead to paralysis. But what if the faulty immune system could be replaced with a new one? Would it still attack the brain's myelin sheath? That’s in essence what researchers at the University of Ottawa asked, and answered.

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A patient holds the medications she takes to slow the progression of her multiple sclerosis​

Neurologist Mark Freedman, a senior scientist at the Ottawa Hospital and professor at the university, said investigators identified two dozen patients with an extremely aggressive early form of MS, for whom all disease-modifying drugs had failed. “Three, four years into your disease, if you saw the wheelchair imminent into your future and someone offered you an alternative, you might consider it," Freedman said. "That’s the kind of population we went after." Critics, he said, argued that the chance of success was poor because such patients are "very resistant to treatment.”

Stem cells purified, returned

Researchers, describing their work in the journal The Lancet, used strong chemotherapy drugs to destroy the patients’ immune systems. At the same time, investigators collected stem cells from each patient’s bone marrow, purified them, and eventually transplanted the cells back into the participants to repopulate their immune systems. “Theoretically," Freedman explained to VOA, "the brand-new immune system no longer carries that memory" of attacking the brain's myelin sheath. Whatever caused the attacks in the first place still isn't known, but the new immune system " won’t have that same problem again.”

The results were as breathtaking as they were unexpected. “Two and three years after the transplant, many of the patients who had significant disability started to recover, recover quite a bit," Freedman said. "So we had patients who were already walking with a cane go back to a life where they were working, they were skating, they were skiing, they’re running, they’re doing everything.”

The results in detail:
 
Sad story of a young couple with cystic fibrosis...
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Terminally ill US couple die days apart
Thu, 22 Sep 2016 - A young married couple who bonded through their shared struggles with cystic fibrosis have both died within days of each other.
A young US married couple who bonded through their shared struggles with cystic fibrosis have both died within days of each other. Katie Prager, 26, died in Kentucky on Thursday, five days after the death of her husband, Dalton Prager, 25. Katie died in bed on Thursday morning, her mother said wrote on Facebook. "I know Dalton was waiting with open arms, as well as both her grandmothers and a host of family and friends that have gone before her," she wrote. The couple married in 2011 after falling in love on Facebook. Doctors had advised against meeting in person, due to the likelihood that Dalton would pass a highly-infectious disease to Katie.

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The young couple on a beach​

The couple had been forced to live in separate states in recent years and were last together for their fifth anniversary in July. Katie had lived in Kentucky, while Dalton was living in Missouri. Cystic fibrosis clogs the lungs with mucus making it difficult for patients to breath. The median survival age is 40-years-old. They had each received lung transplants, which failed. Dalton had tried desperately but was unable to travel to Kentucky to see Katie one last time before his death. "He has tried so many times and he has tried so hard. Unfortunately his body is not agreeing with what he wants to do," his mother Renee Prager told the St Louis Post-Dispatch. The couple raised money for their treatment, and wrote extensively about their difficult experiences.

Lamenting how he and his wife were treated by health insurance companies, Dalton wrote: "They are turning my wife into a number, a statistic, a dollar sign. I cannot lose her! This can't be the end of our love story! "We are both ready to continue fighting but at this point we are running out of options and need your help. Please help me save my wife Katie! "We knew her time was short and she was able to do a few things that she wanted," Katie's mother Debbie wrote. "The days to follow will not be easy but I find comfort in knowing that my girl lived, she really lived." The couple were compared to the one in the book and film The Fault In Our Stars, that focuses on a young couple battling cancer.

Terminally ill US couple die days apart - BBC News
 
MS drug hope for delaying secondary-progressive stage...
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MS drug hope for secondary-progressive stage
23 March 2018 - A study of a new drug to treat advanced cases of multiple sclerosis suggests it may be possible to delay progression of the disease in the short term, although the effects were small.
In a trial of 1,327 people, in The Lancet, 26% saw their disability worsen after three months taking siponimod compared with 32% taking a dummy drug. No drugs currently exist for secondary-progressive multiple sclerosis. An MS expert expressed caution, saying other new treatments were still needed. About 100,000 people in the UK have MS - a lifelong, progressive condition. Most are diagnosed between the ages of 20 and 70.

MS affects the central nervous system and can cause problems with:

* vision
* balance
* fatigue
* stiffness
* memory

Most cases start as relapsing-remitting MS and most of these develop into secondary-progressive MS within 15-20 years.

'Modest effect'

Patients in this trial, which was funded by drug company Novartis, had had MS for an average of 17 years - four years with secondary MS, the advanced stage. Most needed assistance with walking before the trial began. When standard measures of disability were used to track their progress, there was a 21% lower risk of walking or arm movements getting worse for those given the drug, compared with those taking the placebo. But the international research team found the drug had no effect on maintaining patients' walking speed and it had some side-effects, although it was still thought to be safe.

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Siponimod is a pill taken once a day​

Lead author Prof Ludwig Kappos, from the University of Basel, said: "Although the results are not as good as we wanted to see, it is a very large study, which is robust. "It means siponimod is one option to delay the disease in the advanced stage." Dr Susan Kohlhaas, director of research at the MS Society, said: "These results bring us closer to the first ever treatment for people with secondary-progressive MS - so it's big news. "This trial showed that siponimod had a modest but significant effect in slowing disability progression, which is incredibly encouraging."

'Disappointing'

But Dr Luanne Metz, from the University of Calgary, in Canada, said a second trial was needed to confirm the benefits of the drug and its impact beyond three to six months. She said: "Although siponimod seems to reduce the time to confirmed disability in secondary-progressive MS, the treatment effect was small. "In our opinion... the absence of a significant difference for the key secondary clinical outcome are disappointing results and do not suggest that siponimod is an effective treatment for secondary-progressive MS." She added: "Trials of other novel treatments that target non-inflammatory mechanisms are still needed." Before the drug becomes available on the NHS, it would need to be approved by the European Medicines Agency and then recommended as cost-effective by bodies in the UK.

MS drug hope for delaying progression
 

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