Multiple Sclerosis is said to be a disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are impaired, thus resulting in demyelination and scarring in addition to a wide range of signs and symptoms. Scientists from Queen Mary, University of London claim that a new drug for multiple sclerosis seems to exhibit potential in treating the condition suffered by several people in UK.
A chief examination of the oral drug Cladribine has apparently exhibited that it could considerably decrease relapse and worsening of the disease. It may also get rid of the repulsive side effects connected to present therapies. Cladribine is alleged to be the first ever treatment in tablet form for MS, and only requires to be consumed for between 8 to 10 days a year, thereby removing the necessity for usual injections and intravenous infusions otherwise tolerated by sufferers. The effortlessness with which Cladribine tablets may be administered, pooled with its comparatively few side effects, could make it an immensely exhilarating progress in the arena of MS.
Multiple sclerosis is claimed to be an immobilizing neurological condition which typically begins in young adulthood. It supposedly results from the body’s own immune system impairing the central nervous system. This may hamper with the spread of messages between the brain and other portion of the body and may lead to issues with vision, muscle control, hearing and memory. Cladribine tablets supposedly function by repressing the immune system thus curtailing its capability to further assault the central nervous system.
The study was headed by Professor Gavin Giovanonni from Barts and the London School of Medicine and Dentistry. The study included more than 1,300 MS patients who were trailed for almost two years and examined via MRI scans. Patients apparently received either two or four small treatment courses of Cladribine tablets for each year, or a placebo. Every course may comprise of one or two tablets each day for 4 or 5 days, thereby adding up to simply 8 to 20 days of treatment every year.
Professor Giovanonni commented, “The introduction of an oral therapy that is simple and easy to use is a big step forward for people with MS who have been patiently waiting for an oral therapy for decades. The benefits of oral Cladribine as a first line therapy will need to be weighed against the potential long term risks.”
As opposed to patients who were receiving the placebo, those consuming Cladribine tablets appeared to be more than 55 per cent less liable to experience relapse, and around 30 per cent less expected to undergo deterioration in their disability owing to MS.
The study was published online in the New England Journal of Medicine.
Tuesday, April 26, 2011
Novel anti-inflammatory drug allegedly helps treat multiple sclerosis
This piece of investigation stores some good news for patients suffering from multiple sclerosis (MS). A recent research asserts that single injection of the ATL313 compound can treat chronic pain and halt the progression of MS. In this inflammatory disease, the body’s immune system possibly attacks a protective sheath known as myelin that comprises nerves in the spinal cord and brain.
As the disease progresses, myelin presumably develops lesions or scars leading to lifetime neurological problems. Currently available MS medications may decline or block the progression, but fails to treat it. In this research, spinal cord and brain-imaging technology was employed for ascertaining whether rats receiving an ATL313 injection are treated of lesions. It was believed that this class of compounds calm down glial cells in the spinal cord due to their pro-inflammatory activation.
“What’s become evident is that glial cells have a Dr. Jekyll and Mr. Hyde personality. Under normal circumstances they do all these really good things for the neurons, but when they shift into the Mr. Hyde formation they release a whole host of chemicals that cause problems like neuropathic pain and other chronic pain conditions,” said Lisa Loram, a senior research associate in Watkins’ laboratory.
Normally, glial cells seem to be like housekeepers in the nervous system cleaning up debris and being a support for neurons. During the investigations it was noted that glial cells in the central nervous system may also acts as hallmarks in pain improvement. These cells supposedly excite neurons known to transmit pain signals. ATL313 apparently reset the glial cells from an angry activated state to a calm anti-inflammatory state that can heal MS lesions.
The research was presented at the Society for Neuroscience’s annual meeting held in San Diego.
As the disease progresses, myelin presumably develops lesions or scars leading to lifetime neurological problems. Currently available MS medications may decline or block the progression, but fails to treat it. In this research, spinal cord and brain-imaging technology was employed for ascertaining whether rats receiving an ATL313 injection are treated of lesions. It was believed that this class of compounds calm down glial cells in the spinal cord due to their pro-inflammatory activation.
“What’s become evident is that glial cells have a Dr. Jekyll and Mr. Hyde personality. Under normal circumstances they do all these really good things for the neurons, but when they shift into the Mr. Hyde formation they release a whole host of chemicals that cause problems like neuropathic pain and other chronic pain conditions,” said Lisa Loram, a senior research associate in Watkins’ laboratory.
Normally, glial cells seem to be like housekeepers in the nervous system cleaning up debris and being a support for neurons. During the investigations it was noted that glial cells in the central nervous system may also acts as hallmarks in pain improvement. These cells supposedly excite neurons known to transmit pain signals. ATL313 apparently reset the glial cells from an angry activated state to a calm anti-inflammatory state that can heal MS lesions.
The research was presented at the Society for Neuroscience’s annual meeting held in San Diego.
Blocking crucial molecule can purportedly help treat multiple sclerosis
Multiple sclerosis (MS) probably treated by a hypertension drug, is triggered by Granulocyte-macrophage colony-stimulating factor (GM-CSF). Jefferson neuroscientists now claim that simply blocking an important molecule can also aid in fighting MS. Obstructing this cell-signaling molecule appears as the first step in developing new treatments to eradicate the disease.
In the absence of GM-CSF, T helper 17 cells (Th17) cells were supposedly unable to induce the MS-like disease in an experimental animal model. Th17 cells are believed to play a vital pathogenic role in humans and experimental models of autoimmune diseases, but the mechanisms behind this are hazy. In the course of the research, it was suggested that GM-CSF derived from Th17 cells is important in the cell-signaling process that leads to inflammation in the central nervous system.
The interleukin-23 (IL-23)/ Th17/GM-CSF axis seem to be the major pathway in pathogenesis of autoimmune central nervous system inflammation and likely other autoimmune diseases. IL-23 may be a cytokine that leads to autoimmune inflammation of the brain, induces production of more GM-CSF in Th17 cells. An animal model of MS called experimental autoimmune encephalomyelitis (EAE) was used for the investigation.
Abdolmohamad Rostami, M.D., Ph.D., Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, added, “This is the first step towards finding a new treatment. If we can try to neutralize GM-CSF by different means, for example, by trying to mimic it or trying to block the receptor for GM-CSF, we can hopefully ameliorate the disease.”
Mice whose Th17 cells cannot produce GM-CSF possibly failed to develop neuroinflammation. Hence, it can be asserted that GM-CSF is responsible for disease manifestation in this experimental model. Scientists found that the protein interkeukin-27 (IL-27) helped block the onset of symptoms in animals with an MS-like disease. Increasing levels of GM-CSF can trigger the disease, while elevating IL-27 concentrations can supposedly suppress an over-active immune system.
In the absence of GM-CSF, T helper 17 cells (Th17) cells were supposedly unable to induce the MS-like disease in an experimental animal model. Th17 cells are believed to play a vital pathogenic role in humans and experimental models of autoimmune diseases, but the mechanisms behind this are hazy. In the course of the research, it was suggested that GM-CSF derived from Th17 cells is important in the cell-signaling process that leads to inflammation in the central nervous system.
The interleukin-23 (IL-23)/ Th17/GM-CSF axis seem to be the major pathway in pathogenesis of autoimmune central nervous system inflammation and likely other autoimmune diseases. IL-23 may be a cytokine that leads to autoimmune inflammation of the brain, induces production of more GM-CSF in Th17 cells. An animal model of MS called experimental autoimmune encephalomyelitis (EAE) was used for the investigation.
Abdolmohamad Rostami, M.D., Ph.D., Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, added, “This is the first step towards finding a new treatment. If we can try to neutralize GM-CSF by different means, for example, by trying to mimic it or trying to block the receptor for GM-CSF, we can hopefully ameliorate the disease.”
Mice whose Th17 cells cannot produce GM-CSF possibly failed to develop neuroinflammation. Hence, it can be asserted that GM-CSF is responsible for disease manifestation in this experimental model. Scientists found that the protein interkeukin-27 (IL-27) helped block the onset of symptoms in animals with an MS-like disease. Increasing levels of GM-CSF can trigger the disease, while elevating IL-27 concentrations can supposedly suppress an over-active immune system.
leukemia drug treat multiple sclerosis?
A novel study by researchers at the University of Cambridge unearthed some rather interesting results. The study suggests that a drug commonly used to treat leukemia called alemtuzumab could also help in the treatment of patients with multiple sclerosis (MS).
An original treatment drug for leukemia, Genzyme Corp has patent rights to the monoclonal antibody alemtuzumab drug. Clinical trials of the drug showed that it had the potential to turn over and in some cases even put an end to the crippling effects of MS. On the face of it alemtuzumab was found to repair damaged tissues in the brain, consequently reducing the disability of the patients.
It also lowered the number of attacks the MS patients suffered and gave them a greater ability to bring back their lost functions.
Study author, Lee Dunster, mentioned, “This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in, day out.”
Coordinating many aspects of the study, Dr Alasdair Coles, lecturer for department of clinical neurosciences at Cambridge University, further remarked, “The ability of an MS drug to promote brain repair is unprecedented. We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue.”
In order to study the influence of the drug, researchers conducted clinical trails that involved nearly 334 patients diagnosed with early-stage relapsing-remitting MS. These individuals had never before been treated with alemtuzumab or interferon beta-1a. The mentioned drugs are one of the most effective licensed therapies for similar MS cases.
Funded in part by Genzyme Corp, the three year study discovered that patients had 74% lowered down the rack feeling as against other treatment methods. They also had reduced risks of sustained accumulation of disability by 71% over interferon beta-1a. The researchers mention the results are promising as the drug not only reduced the suffering of MS patients but also helped them get back some of their physical and intellectual functions. While disabilities in other patients who were off alemtuzumab saw a worsening in terms of their disability, the other patients showed improvement in their disability.
Affecting millions of people all over the globe with nearly 100,000 in Britain and 400,000 in the United States alone, MS is a type of auto-immune disease that has practically no cure and very few methods of effective treatment. Characterized by the body’s immune system attacking nerve fibres in the central nervous system, the debilitating condition can eventually lead to fatigue, cognitive problems, depresion and loss of sight and movement.
The Phase II of the clinical trial reveals great potential for the drug to treat MS patients. Let’s hope this one has some good news for the millions affected by MS.
An original treatment drug for leukemia, Genzyme Corp has patent rights to the monoclonal antibody alemtuzumab drug. Clinical trials of the drug showed that it had the potential to turn over and in some cases even put an end to the crippling effects of MS. On the face of it alemtuzumab was found to repair damaged tissues in the brain, consequently reducing the disability of the patients.
It also lowered the number of attacks the MS patients suffered and gave them a greater ability to bring back their lost functions.
Study author, Lee Dunster, mentioned, “This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in, day out.”
Coordinating many aspects of the study, Dr Alasdair Coles, lecturer for department of clinical neurosciences at Cambridge University, further remarked, “The ability of an MS drug to promote brain repair is unprecedented. We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue.”
In order to study the influence of the drug, researchers conducted clinical trails that involved nearly 334 patients diagnosed with early-stage relapsing-remitting MS. These individuals had never before been treated with alemtuzumab or interferon beta-1a. The mentioned drugs are one of the most effective licensed therapies for similar MS cases.
Funded in part by Genzyme Corp, the three year study discovered that patients had 74% lowered down the rack feeling as against other treatment methods. They also had reduced risks of sustained accumulation of disability by 71% over interferon beta-1a. The researchers mention the results are promising as the drug not only reduced the suffering of MS patients but also helped them get back some of their physical and intellectual functions. While disabilities in other patients who were off alemtuzumab saw a worsening in terms of their disability, the other patients showed improvement in their disability.
Affecting millions of people all over the globe with nearly 100,000 in Britain and 400,000 in the United States alone, MS is a type of auto-immune disease that has practically no cure and very few methods of effective treatment. Characterized by the body’s immune system attacking nerve fibres in the central nervous system, the debilitating condition can eventually lead to fatigue, cognitive problems, depresion and loss of sight and movement.
The Phase II of the clinical trial reveals great potential for the drug to treat MS patients. Let’s hope this one has some good news for the millions affected by MS.
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