When mice with moderate multiple sclerosis were given very low dosages of dextromethorphan, a drug found in cough medicine, the loss of myelin and the development of paralysis during acute attacks was significantly reduced. (Credit: iStockphoto)
UC DAVIS (US) — A drug commonly found in over-the-counter cough medicine may pave the way for a new and inexpensive therapy for multiple sclerosis.
23Share
In animal testing, the drug dextromethorphan significantly reduced the loss of the fatty sheath (or myelin) surrounding nerve fibers in the central nervous system and also minimized development of paralysis during multiple sclerosis attacks.
The study is published online in the journal Neurobiology of Disease.
“This finding provides an exciting opportunity to better understand the disease and to pursue a new treatment strategy with a drug that is widely available, inexpensive, and known to be safe,” says Wenbin Deng, assistant professor of cell biology and human anatomy at University of California, Davis.
Currently there are few effective treatment options for multiple sclerosis, which affects about 400,000 people in the United States and most often first appears in young-to-middle-aged women.
The condition, that has no cure, is caused by cells of the immune system attacking myelin, the fatty sheath surrounding nerve fibers in the central nervous system that speeds the transmission of nerve impulses.
Symptoms vary widely and often involve periods of motor problems, including paralysis of a limb or poor coordination, which unpredictably may either go away or become permanent. As the disease progresses, it causes increasing disability. Many treatments are poorly tolerated and produce a wide range of side effects.
For the new study, investigators induced mice to have either a moderate or severe type of multiple sclerosis and then treated them with either very low or high dosages of dextromethorphan. Very low dosages given to mice with moderate disease significantly reduced the loss of myelin and the development of paralysis during acute attacks. The high dosages did not offer any benefit.
“Finding that a chemical like dextromethorphan might be useful for treating multiple sclerosis is especially significant because we already know it is safe,” says David E. Pleasure, director of research at the Institute for Pediatric Regenerative Medicine at Shriners Hospitals for Children Northern California in Sacramento and one of the authors of the study. “Normally, a possible new treatment must first undergo years of clinical trials to prove this.”
The researchers began investigating common, over-the-counter cough medicines as treatments for devastating diseases like multiple sclerosis because their molecular structure is similar to morphine. Morphinans—low dose morphine-like agents—have been used “off label” for individuals. While they’re not cures, they potentially can be helpful for selected patients, and appear to have little or no toxicity at low doses.
Dextromethorphan is one of a few morphinan drugs similar in structure to morphine, but without the addictive properties. Deng and Pleasure would like to see clinical trials conducted soon to find out if dextromethorphan is effective in humans with multiple sclerosis. Such a trial would likely involve testing in combination with current standard treatment of the disease.
“Dextromethorphan has a different mode of action than current drugs for multiple sclerosis,” Deng says. “While current treatment targets inflammation and the immune system, dextromethorphan appears to be more directly neuroprotective. Combining the different strategies could offer a real breakthrough in fighting the disease.”
The study was supported in part by grants from the National Institutes of Health, National Multiple Sclerosis Society, and Shriners Hospitals for Children.
Thursday, July 14, 2011
Thursday, June 30, 2011
The Hubbard Foundation
USA: The Hubbard Foundation - CCSVI Treatment
The Hubbard Foundation has an IRB-approved study to test CCSVI and treat CCSVI. Those with positive results for CCSVI according to the Haacke Protocol with the Hubbard Foundation, are referred for catheter venoography and if positive for balloon venoplasty.
The Interventional Radiologists (IRs) are Justin Gooding MD, Donald Ponec MD, Richard Saxon MD,
The IRs work out of a private vein clinic in Del Mar, San Diego, CA called MIT Del Mar Vein Care. The MIT Del Mar staff prefers to answer all questions pertaining to CCSVI treatment and treatment fees.
To contact MIT Del Mar Vein Care go to: http://delmarveincare.com/contact.htm
The Hubbard Foundation is mainly a research facility. The primary form of contact is via e-mail: hubbardfoundation@gmail.com or Fax: (858)444-3599
To schedule CCSVI testing and treatment visit:
The Hubbard Foundation
10065 Old Grove Rd. Suite 103
San Diego, CA 92131
The Hubbard Foundation has an IRB-approved study to test CCSVI and treat CCSVI. Those with positive results for CCSVI according to the Haacke Protocol with the Hubbard Foundation, are referred for catheter venoography and if positive for balloon venoplasty.
The Interventional Radiologists (IRs) are Justin Gooding MD, Donald Ponec MD, Richard Saxon MD,
The IRs work out of a private vein clinic in Del Mar, San Diego, CA called MIT Del Mar Vein Care. The MIT Del Mar staff prefers to answer all questions pertaining to CCSVI treatment and treatment fees.
To contact MIT Del Mar Vein Care go to: http://delmarveincare.com/contact.htm
The Hubbard Foundation is mainly a research facility. The primary form of contact is via e-mail: hubbardfoundation@gmail.com or Fax: (858)444-3599
To schedule CCSVI testing and treatment visit:
http://hubbardfoundation.org/index.html
The Hubbard Foundation
10065 Old Grove Rd. Suite 103
San Diego, CA 92131
Beet Juice and the brain
Beet Juice Good for Brain
www.webmd.com
Drinking beet juice increases blood flow to the brain in older adults, a finding that suggests that consumption of the liquid in the dark red vegetable holds potential for fighting the progression of dementia, a new study says.
www.webmd.com
Drinking beet juice increases blood flow to the brain in older adults, a finding that suggests that consumption of the liquid in the dark red vegetable holds potential for fighting the progression of dementia, a new study says.
Wednesday, June 29, 2011
Canadian MS News
CTV.ca News Staff
Date: Wed. Jun. 29 2011 4:27 PM ET
The federal government says it will fund clinical trials into the controversial multiple sclerosis treatment known as the "liberation therapy."
Federal Health Minister Leona Aglukkaq made the announcement Wednesday afternoon during a news conference on Parliament Hill.
Aglukkaq told reporters the government came to its decision after a scientific working group it convened last summer determined during a meeting on Tuesday that a Phase 1 and Phase 2 clinical trial should proceed.
"I have asked CIHR, the Canadian Institute of Health Research, to establish the terms of reference for this clinical trial," Aglukkaq said. "And we are committed to launching an open and transparent call for proposals, and process applications, as quickly as possible."
The liberation treatment was developed by Italian physician Dr. Paolo Zamboni and is based on his theory that narrowed neck veins are behind MS symptoms.
The condition, chronic cerebrospinal venous insufficiency, or CCSVI, reduces blood flow and allows iron deposits to build up in the brain, Zamboni says.
The treatment he developed uses balloon angioplasty to unblock the veins in the hope of alleviating symptoms.
While Zamboni's research has demonstrated success with the treatment, recent clinical trials have concluded that CCSVI is not a primary cause of MS.
The controversy surrounding both the condition and the treatment has not deterred Canadian MS patients from rallying across the country over the last several months to call on both Ottawa and provincial governments to fund the treatment, which is not available in Canada. Many Canadians have had the procedure at medical clinics overseas.
Aglukkaq said the working group was established last August and tasked with reviewing the latest research and making its recommendation to government. The group met in November and again on Tuesday.
Dr. Alain Beaudet, president of the Canadian Institutes of Health Research, said Wednesday that an analysis of all the research done on CCSVI so far suggested "a trend to an association between the greater prevalence of CCSVI in patients with MS than in healthy controls."
Beaudet said more results are needed, particularly from seven current studies, to strengthen the committee's conclusion.
"But, nonetheless, the committee felt that, on the basis of this preliminary evidence and what's published so far, that we should in parallel start already with a Phase 1-2 trial," he said.
During her Wednesday news conference, Aglukkaq hailed MS patients and their families for their struggle with a disease that can lead to symptoms that include difficulty walking, vision problems, fatigue and weakness.
"It has been a moving experience to meet many of you and to hear from so many MS patients and their families who have shown tremendous courage in the face of such difficult illness," she said.
Date: Wed. Jun. 29 2011 4:27 PM ET
The federal government says it will fund clinical trials into the controversial multiple sclerosis treatment known as the "liberation therapy."
Federal Health Minister Leona Aglukkaq made the announcement Wednesday afternoon during a news conference on Parliament Hill.
Aglukkaq told reporters the government came to its decision after a scientific working group it convened last summer determined during a meeting on Tuesday that a Phase 1 and Phase 2 clinical trial should proceed.
"I have asked CIHR, the Canadian Institute of Health Research, to establish the terms of reference for this clinical trial," Aglukkaq said. "And we are committed to launching an open and transparent call for proposals, and process applications, as quickly as possible."
The liberation treatment was developed by Italian physician Dr. Paolo Zamboni and is based on his theory that narrowed neck veins are behind MS symptoms.
The condition, chronic cerebrospinal venous insufficiency, or CCSVI, reduces blood flow and allows iron deposits to build up in the brain, Zamboni says.
The treatment he developed uses balloon angioplasty to unblock the veins in the hope of alleviating symptoms.
While Zamboni's research has demonstrated success with the treatment, recent clinical trials have concluded that CCSVI is not a primary cause of MS.
The controversy surrounding both the condition and the treatment has not deterred Canadian MS patients from rallying across the country over the last several months to call on both Ottawa and provincial governments to fund the treatment, which is not available in Canada. Many Canadians have had the procedure at medical clinics overseas.
Aglukkaq said the working group was established last August and tasked with reviewing the latest research and making its recommendation to government. The group met in November and again on Tuesday.
Dr. Alain Beaudet, president of the Canadian Institutes of Health Research, said Wednesday that an analysis of all the research done on CCSVI so far suggested "a trend to an association between the greater prevalence of CCSVI in patients with MS than in healthy controls."
Beaudet said more results are needed, particularly from seven current studies, to strengthen the committee's conclusion.
"But, nonetheless, the committee felt that, on the basis of this preliminary evidence and what's published so far, that we should in parallel start already with a Phase 1-2 trial," he said.
During her Wednesday news conference, Aglukkaq hailed MS patients and their families for their struggle with a disease that can lead to symptoms that include difficulty walking, vision problems, fatigue and weakness.
"It has been a moving experience to meet many of you and to hear from so many MS patients and their families who have shown tremendous courage in the face of such difficult illness," she said.
Friday, May 20, 2011
Doctor Hubbard theory of MS
Dr. Hubbard's theory of MS
Dr. David Hubbard is a neurologist and founder of the Hubbard fMRI Institute and the Hubbard Foundation. He, and Dr. Jack Burks, were the only neurologists present at the recent CCSVI conference, although many neurologists were invited to attend. This was disappointing, to say the least. One would assume that neurologists would be interested in new research into the blood brain barrier and MS. The first thing to note is that the current theory of MS is still only a THEORY. There is absolutely no proof that rogue t-cells are what cause MS. This is an hypothesis. Dr. Hubbard began by discussing the current autoimmune theory. MS drugs, based on EAE and this theory, have a 30% efficacy rate...about the same as placebo. The reason MS drug trials have to be so large and involve so many participants is that it takes that many people to make any statistical significance. The MS drugs are not a success story. They do NOT prove the autoimmune hypothesis. Dr. Hubbard presented his very important insight into what he believes is causing the white matter lesions and destruction of myelin in the MS brain. It is very different than the current understanding that MS specialists propose with the EAE mouse model and the idea that myelin destruction is caused by an out of control immune system which is attacking itself. Oligodendrocytes are a type of brain cell which form the covering of our axons. They make up the myelin sheath. Dr. Hubbard cites research of Prineas and Barnett, showing that the oligodendrocytes DIE FIRST in MS. They are not dying because of an immune attack of white cells....they die BEFORE the immune system is ever involved. The ologodendrocyte shrinks and dies from the center of the cell. Only later do t-cells come in clean up. Macrophages also come in to clean up, this is a standard response of the body to tissue death. "White cells just don't go chomping on the blood brain barrier...they are invited in." So what is the "unknown factor" that is killing oligodendrocytes and inviting in white cells??? Dr. Hubbard proposes that this "unknown factor" is decreased perfusion, or slowed blood flow thru the brain. (Fans of the page will note that this has been the theory of Marie and myself, too, since the beginning of our journey.) Here's an earlier note on hypoperfusion and MS https://www.facebook.com/note.php?note_id=439394977210 The fMRI studies and Dr. Haacke's blood flow studies are confirming this theory. The thing about perfusion is that it affects both WHITE and GRAY matter. It is affects the ENTIRE BRAIN. MS is a disease of the entire brain....gray matter atrophy and white matter demylination. This theory is the first to address BOTH ASPECTS. White cells are picked up by the edges of the endothelium, roll along and then are invited thru the tight junction to get into the brain's paranchyma. MS is not a disease of an immune system gone awry. It is a disease where white blood cells are responding to injury, and are acting appropriately. CCSVI creates a slowed perfusion, or slow flow of blood in the brain. Decreased perfusion and reduced flow and stagnation in the vein causes a shunting of blood around the abnormal venule, the oligodendrocyte is not getting enough O2 and glucose. The oligodendorcyte dies. Please watch all of Dr. Hubbard's research and listen closely. I believe that this is the answer, and connects all we KNOW and all we can SEE about MS brains. http://www.youtube.com/user/HubbFound#p/u/39/Z1BP_xOQQlY I believe this is MS.... - I thank Dr. David Hubbard for bringing the pieces together as a neurologist. - I thank Marie Rhodes for bringing the pieces together as a medical writer. www.ccsvibook.com And I thank all the researchers who are ready to look at this new theory, take it further and begin the process of ENDING MS. For good. Joan
By: CCSVI in Multiple Sclerosis
Dr. David Hubbard is a neurologist and founder of the Hubbard fMRI Institute and the Hubbard Foundation. He, and Dr. Jack Burks, were the only neurologists present at the recent CCSVI conference, although many neurologists were invited to attend. This was disappointing, to say the least. One would assume that neurologists would be interested in new research into the blood brain barrier and MS. The first thing to note is that the current theory of MS is still only a THEORY. There is absolutely no proof that rogue t-cells are what cause MS. This is an hypothesis. Dr. Hubbard began by discussing the current autoimmune theory. MS drugs, based on EAE and this theory, have a 30% efficacy rate...about the same as placebo. The reason MS drug trials have to be so large and involve so many participants is that it takes that many people to make any statistical significance. The MS drugs are not a success story. They do NOT prove the autoimmune hypothesis. Dr. Hubbard presented his very important insight into what he believes is causing the white matter lesions and destruction of myelin in the MS brain. It is very different than the current understanding that MS specialists propose with the EAE mouse model and the idea that myelin destruction is caused by an out of control immune system which is attacking itself. Oligodendrocytes are a type of brain cell which form the covering of our axons. They make up the myelin sheath. Dr. Hubbard cites research of Prineas and Barnett, showing that the oligodendrocytes DIE FIRST in MS. They are not dying because of an immune attack of white cells....they die BEFORE the immune system is ever involved. The ologodendrocyte shrinks and dies from the center of the cell. Only later do t-cells come in clean up. Macrophages also come in to clean up, this is a standard response of the body to tissue death. "White cells just don't go chomping on the blood brain barrier...they are invited in." So what is the "unknown factor" that is killing oligodendrocytes and inviting in white cells??? Dr. Hubbard proposes that this "unknown factor" is decreased perfusion, or slowed blood flow thru the brain. (Fans of the page will note that this has been the theory of Marie and myself, too, since the beginning of our journey.) Here's an earlier note on hypoperfusion and MS https://www.facebook.com/note.php?note_id=439394977210 The fMRI studies and Dr. Haacke's blood flow studies are confirming this theory. The thing about perfusion is that it affects both WHITE and GRAY matter. It is affects the ENTIRE BRAIN. MS is a disease of the entire brain....gray matter atrophy and white matter demylination. This theory is the first to address BOTH ASPECTS. White cells are picked up by the edges of the endothelium, roll along and then are invited thru the tight junction to get into the brain's paranchyma. MS is not a disease of an immune system gone awry. It is a disease where white blood cells are responding to injury, and are acting appropriately. CCSVI creates a slowed perfusion, or slow flow of blood in the brain. Decreased perfusion and reduced flow and stagnation in the vein causes a shunting of blood around the abnormal venule, the oligodendrocyte is not getting enough O2 and glucose. The oligodendorcyte dies. Please watch all of Dr. Hubbard's research and listen closely. I believe that this is the answer, and connects all we KNOW and all we can SEE about MS brains. http://www.youtube.com/user/HubbFound#p/u/39/Z1BP_xOQQlY I believe this is MS.... - I thank Dr. David Hubbard for bringing the pieces together as a neurologist. - I thank Marie Rhodes for bringing the pieces together as a medical writer. www.ccsvibook.com And I thank all the researchers who are ready to look at this new theory, take it further and begin the process of ENDING MS. For good. Joan
By: CCSVI in Multiple Sclerosis
Tuesday, May 17, 2011
Skip Navigation LinksHome > April 21, 2011 - Volume 11 - Issue 8 > Skyrocketing MS Drug Prices Hit Patients Hard, Prompting Com...
< Previous Article | Next Article >
Neurology Today:
21 April 2011 - Volume 11 - Issue 8 - pp 1,19,23
doi: 10.1097/01.NT.0000397957.19762.cd
Features
Skyrocketing MS Drug Prices Hit Patients Hard, Prompting Compliance Problems
Shaw, Gina
Back to Top | Article Outline
ARTICLE IN BRIEF
Neurologists are experiencing the fallout from the steep rise in the cost of MS drugs: Many patients are finding it difficult to comply with their therapy regimen. Among solutions, they recommend governmental intervention in negotiating prices.
AS NEWER, MORE EXPEN...
AS NEWER, MORE EXPEN...
Image Tools
When the first oral drug for multiple sclerosis, fingolimod (Gilenya), first entered the market last fall, neurologists and patients alike experienced sticker shock: the medication was priced at a jaw-dropping $48,000 a year. But, some pointed out, it was the first drug of its kind, with no direct competitors. Perhaps it shouldn‘t be surprising that it came at a premium.
And then the price hikes for other MS drugs followed. Teva's glatiramer (Copaxone) now comes at a rack rate of over $42,000 per year — a jump of nearly 40 percent over prices at the beginning of 2010. Biogen has also raised prices further for both natalizumab (Tysabri) and interferon-beta-1a (Avonex).
Why should older drugs — whose existing prices, one assumes, were already set to cover the costs of bringing the drugs to market in the first place — get a price increase when a new drug comes to market?
Companies want to get the most out of their investment, said Edward Fox, MD, PhD, clinical associate professor of neurology at the University of Texas Medical Branch and director of the MS Clinic of Central Texas. “With the onset of new medications that come at a premium, companies have raised the price of older medications in order not to appear inferior to the new drugs. They look at the price as being meaningful when it comes to expectations. If a certain drug is priced lowest, it must be less worthy somehow.”
Of course, virtually no patients are paying out of pocket the full listed price for these costly medications. “I have 1,400 MS patients and I don‘t have single patient paying full price. I can‘t even conceive of someone with a salary high enough where that would be a consideration,” Dr. Fox said.
But the price increases are still driving more and more people with MS and their families into desperate situations. That's because as the prices paid by third-party insurers have gone up, so too have patients‘ copays and other shared costs. “On a weekly basis, I‘m dealing with patients who have what I would call a medication crisis,” Dr. Fox said. “Many of my patients have copays of between $300 and $800 a month. There aren‘t too many families who can easily absorb that cost.”
Bruce A. Cohen, MD, professor of neurology and director of the Comprehensive Multiple Sclerosis Program at Northwestern University's Feinberg School of Medicine, said that he has a number of patients who are making treatment decisions based primarily on cost.
But that's getting harder and harder to do, said Dr. Fox: “It's become an across the board situation where all of the MS medications are so expensive that you can‘t just switch to a less costly alternative.”
< Previous Article | Next Article >
Neurology Today:
21 April 2011 - Volume 11 - Issue 8 - pp 1,19,23
doi: 10.1097/01.NT.0000397957.19762.cd
Features
Skyrocketing MS Drug Prices Hit Patients Hard, Prompting Compliance Problems
Shaw, Gina
Back to Top | Article Outline
ARTICLE IN BRIEF
Neurologists are experiencing the fallout from the steep rise in the cost of MS drugs: Many patients are finding it difficult to comply with their therapy regimen. Among solutions, they recommend governmental intervention in negotiating prices.
AS NEWER, MORE EXPEN...
AS NEWER, MORE EXPEN...
Image Tools
When the first oral drug for multiple sclerosis, fingolimod (Gilenya), first entered the market last fall, neurologists and patients alike experienced sticker shock: the medication was priced at a jaw-dropping $48,000 a year. But, some pointed out, it was the first drug of its kind, with no direct competitors. Perhaps it shouldn‘t be surprising that it came at a premium.
And then the price hikes for other MS drugs followed. Teva's glatiramer (Copaxone) now comes at a rack rate of over $42,000 per year — a jump of nearly 40 percent over prices at the beginning of 2010. Biogen has also raised prices further for both natalizumab (Tysabri) and interferon-beta-1a (Avonex).
Why should older drugs — whose existing prices, one assumes, were already set to cover the costs of bringing the drugs to market in the first place — get a price increase when a new drug comes to market?
Companies want to get the most out of their investment, said Edward Fox, MD, PhD, clinical associate professor of neurology at the University of Texas Medical Branch and director of the MS Clinic of Central Texas. “With the onset of new medications that come at a premium, companies have raised the price of older medications in order not to appear inferior to the new drugs. They look at the price as being meaningful when it comes to expectations. If a certain drug is priced lowest, it must be less worthy somehow.”
Of course, virtually no patients are paying out of pocket the full listed price for these costly medications. “I have 1,400 MS patients and I don‘t have single patient paying full price. I can‘t even conceive of someone with a salary high enough where that would be a consideration,” Dr. Fox said.
But the price increases are still driving more and more people with MS and their families into desperate situations. That's because as the prices paid by third-party insurers have gone up, so too have patients‘ copays and other shared costs. “On a weekly basis, I‘m dealing with patients who have what I would call a medication crisis,” Dr. Fox said. “Many of my patients have copays of between $300 and $800 a month. There aren‘t too many families who can easily absorb that cost.”
Bruce A. Cohen, MD, professor of neurology and director of the Comprehensive Multiple Sclerosis Program at Northwestern University's Feinberg School of Medicine, said that he has a number of patients who are making treatment decisions based primarily on cost.
But that's getting harder and harder to do, said Dr. Fox: “It's become an across the board situation where all of the MS medications are so expensive that you can‘t just switch to a less costly alternative.”
WHY NOT PUT IT OUT NOW ON THOSE WHO WIILL RISK IT ?
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SA Time: Wednesday, May 18, 2011 12:30:33 AM
Drug that could stop MS discovered
May 9 2011 at 09:24pm
By Fiona Macrae
Copy of st lab
.
Breakthrough: Scientists are hopeful that they ve found a way of stopping multiple sclerosis in its tracks
Related Stories
Vitamin D linked to minimal MS risk - study
London - A drug that could stop multiple sclerosis in its tracks has been discovered by scientists.
In a major breakthrough in the battle against the devastating disease, researchers have pinpointed the chemical “driving force” behind MS.
Without it, the disease does not develop. And when it is mopped up, symptoms are greatly eased, even in brains already ravaged by the illness.
The results come from experiments on mice but the researchers say they are “quietly optimistic” that taking the same tack will help people with MS. The first trials on patients are pencilled in for later this year.
The debilitating condition affects 2.5 million people around the world, and can cause blindness and paralysis. Current drugs are not suitable for all and there is no cure.
The excitement centres on two studies published recently which show an immune system chemical called GM-CSF to be the “vital piece in the jigsaw” of MS.
In the healthy body, it is part of our defence against disease, attacking viruses and other invaders. But in MS, it triggers a series of reactions that culminate in “scavenger cells” destroying myelin - the fatty protective sheath around nerve fibres in the brain and spinal cord - which disrupts the transmission of messages from the brain.
When Swiss researcher Burkhard Becher gave an antibody that counters GM-CSF to mice with an MS-like condition, it greatly improved their health.
Professor Becher, of the University of Zurich, said: “It is relatively easy to stop mice from getting the disease, so we waited until they had the disease and were pretty sick. This is similar to the clinical situation - patients don’t go to the doctor because they think they might get MS, they go when they have MS.”
The drug was also given to mice whose disease was similar to the most common form of MS, in which relapses are followed by periods of remission. Here, mopping up the GM-CSF prevented any further relapses, the journal Nature Immunology reports.
Becher said: “We are extremely hopeful but whether this form of therapy will actually help MS patients remains to be seen. Quiet optimism is the way to go.
“I am not sure this is going to work in patients but, based on the mouse data, I believe GM-CSF is a good thing to target.”
A German firm, which has no connections to the professor, is already trying to use antibodies against the chemical to treat rheumatoid arthritis. It plans to start tests on MS patients at the end of this year.
It usually takes at least seven years from when a drug is first tried out on patients until it hits the market.
A second study, from Thomas Jefferson University in Philadelphia, also points the finger at GM-CSF.
Although the chemical was known to play a role in MS, its pivotal contribution was not understood until now.
“This is a very interesting development,” said Dr Doug Brown, of the MS Society in the UK. “It is early days and there is still a lot of work to be done before we fully understand what it means for people with MS, but it is satisfying to see that trials are already planned and we look forward to seeing how these progress.”
Mopping up excess GM-CSF may also help treat other conditions, including diabetes, it is hoped. – Daily Mail
Take a break
Subscribe to our new Lifestyle newsletter!
Coffee cup
Advanced Search
IOL - logo Home
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Family
Food & Drink
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Style
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Travel
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Games
GQ
SA Time: Wednesday, May 18, 2011 12:30:33 AM
Drug that could stop MS discovered
May 9 2011 at 09:24pm
By Fiona Macrae
Copy of st lab
.
Breakthrough: Scientists are hopeful that they ve found a way of stopping multiple sclerosis in its tracks
Related Stories
Vitamin D linked to minimal MS risk - study
London - A drug that could stop multiple sclerosis in its tracks has been discovered by scientists.
In a major breakthrough in the battle against the devastating disease, researchers have pinpointed the chemical “driving force” behind MS.
Without it, the disease does not develop. And when it is mopped up, symptoms are greatly eased, even in brains already ravaged by the illness.
The results come from experiments on mice but the researchers say they are “quietly optimistic” that taking the same tack will help people with MS. The first trials on patients are pencilled in for later this year.
The debilitating condition affects 2.5 million people around the world, and can cause blindness and paralysis. Current drugs are not suitable for all and there is no cure.
The excitement centres on two studies published recently which show an immune system chemical called GM-CSF to be the “vital piece in the jigsaw” of MS.
In the healthy body, it is part of our defence against disease, attacking viruses and other invaders. But in MS, it triggers a series of reactions that culminate in “scavenger cells” destroying myelin - the fatty protective sheath around nerve fibres in the brain and spinal cord - which disrupts the transmission of messages from the brain.
When Swiss researcher Burkhard Becher gave an antibody that counters GM-CSF to mice with an MS-like condition, it greatly improved their health.
Professor Becher, of the University of Zurich, said: “It is relatively easy to stop mice from getting the disease, so we waited until they had the disease and were pretty sick. This is similar to the clinical situation - patients don’t go to the doctor because they think they might get MS, they go when they have MS.”
The drug was also given to mice whose disease was similar to the most common form of MS, in which relapses are followed by periods of remission. Here, mopping up the GM-CSF prevented any further relapses, the journal Nature Immunology reports.
Becher said: “We are extremely hopeful but whether this form of therapy will actually help MS patients remains to be seen. Quiet optimism is the way to go.
“I am not sure this is going to work in patients but, based on the mouse data, I believe GM-CSF is a good thing to target.”
A German firm, which has no connections to the professor, is already trying to use antibodies against the chemical to treat rheumatoid arthritis. It plans to start tests on MS patients at the end of this year.
It usually takes at least seven years from when a drug is first tried out on patients until it hits the market.
A second study, from Thomas Jefferson University in Philadelphia, also points the finger at GM-CSF.
Although the chemical was known to play a role in MS, its pivotal contribution was not understood until now.
“This is a very interesting development,” said Dr Doug Brown, of the MS Society in the UK. “It is early days and there is still a lot of work to be done before we fully understand what it means for people with MS, but it is satisfying to see that trials are already planned and we look forward to seeing how these progress.”
Mopping up excess GM-CSF may also help treat other conditions, including diabetes, it is hoped. – Daily Mail
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