Chicago actor Jeremy Piven has unexpectedly left the cast of the Broadway revival of "Speed-the-Plow" because of a mercury count that his doctor said was the highest level he'd ever seen.
Piven, 43, wanted to continue but he was advised to stop. Dr. Carlon Colker, who had been treating Piven, said Piven was suffering from "extreme mercury toxicity" and that "a test revealed that Jeremy had ... six times a healthy amount of mercury in his system." Piven has long been a sushi eater, often twice a day, which may be the ultimate cause of the problem.
A major symptom of mercury poisoning is extreme fatigue. Piven was also experiencing neuro-muscular dysfunction, which resulted in his having trouble lifting his arms and legs.
Piven has won Emmy Awards for his role as foul-mouthed Hollywood agent Ari Gold in the HBO series Entourage. He had been performing to critical praise in "Speed-the-Plow" since October.
http://articles.mercola.com/sites/articles/archive/2009/01/06/extreme-mercury-toxicity-sidelines-actor-jeremy-piven.aspx
mercredi 7 janvier 2009
lundi 10 novembre 2008
Another Tysabri patient has PML
boston.com
Todd Wallack
Globe Staff / October 30, 2008
Biogen Idec Inc. reported late yesterday that another patient contracted a potentially fatal brain disease after taking the multiple sclerosis drug Tysabri, the third case since the biotechnology giant reintroduced the treatment two years ago. The news sent shares tumbling 12.1 percent in after-hours trading.
The Cambridge company originally launched Tysabri in 2004, but pulled it from the market just three months later after a few patients were diagnosed with progressive multifocal leukoencephalopathy, or PML. Two died. The company reintroduced Tysabri with its Irish partner, Elan Corp., in July 2006 with stricter prescribing guidelines - designed to minimize the risk of contracting the disease - and a warning that one in 1,000 patients could contract PML.
Three months ago, Biogen Idec said two additional patients had contracted PML, sparking fears that some doctors and patients will decide Tysabri isn't worth the risk.
But despite the chance of contracting the disease, many patients have been willing to use Tysabri to treat serious forms of MS and Crohn's disease when other treatments fail. As of the end of September, more than 35,500 patients were taking Tysabri, and Biogen Idec predicts 100,000 will use the drug by 2010.
Biogen Idec provided few details about the latest PML case, saying only the patient is receiving medical care.
Todd Wallack
Globe Staff / October 30, 2008
Biogen Idec Inc. reported late yesterday that another patient contracted a potentially fatal brain disease after taking the multiple sclerosis drug Tysabri, the third case since the biotechnology giant reintroduced the treatment two years ago. The news sent shares tumbling 12.1 percent in after-hours trading.
The Cambridge company originally launched Tysabri in 2004, but pulled it from the market just three months later after a few patients were diagnosed with progressive multifocal leukoencephalopathy, or PML. Two died. The company reintroduced Tysabri with its Irish partner, Elan Corp., in July 2006 with stricter prescribing guidelines - designed to minimize the risk of contracting the disease - and a warning that one in 1,000 patients could contract PML.
Three months ago, Biogen Idec said two additional patients had contracted PML, sparking fears that some doctors and patients will decide Tysabri isn't worth the risk.
But despite the chance of contracting the disease, many patients have been willing to use Tysabri to treat serious forms of MS and Crohn's disease when other treatments fail. As of the end of September, more than 35,500 patients were taking Tysabri, and Biogen Idec predicts 100,000 will use the drug by 2010.
Biogen Idec provided few details about the latest PML case, saying only the patient is receiving medical care.
lundi 3 novembre 2008
Traitements de choc pour la sclérose en plaques
Ouest France
mercredi 29 octobre 2008
Deux médicaments donnent des résultats deux fois plus efficaces pour contrôler l'évolution de la maladie. Mais ils sont très agressifs.
Une lueur d'espoir ? « Administré suffisamment tôt, le Campath pourrait efficacement stopper l'avancée de la maladie et rétablir des fonctions perdues en favorisant la reconstitution du tissu cérébral endommagé », assure le docteur Alastair Coles (Université de Cambridge).
La sclérose en plaques (SEP) est une maladie incurable du système nerveux, qui touche 80 000 personnes en France. Un dysfonctionnement du système immunitaire provoque la destruction de la myéline qui entoure les nerfs, conduisant à des handicaps plus ou moins lourds (baisse d'acuité visuelle, fatigue, troubles de l'humeur, paralysies partielles...).
L'étude britannique, publiée dans le New England Journal of Medicine, a porté sur 334 patients souffrant d'une forme agressive de la SEP à un stade précoce. Comparé au médicament de référence (Interféron beta-1a), le Campath a montré des résultats deux fois supérieurs. Pourtant, les précédents essais, sur des patients à des stades avancés de la maladie, avaient été des échecs.
Des résultats à Rennes
Au CHU de Rennes, le professeur Gilles Edan a contribué à une étude franco-italienne qui donne des résultats approchants, avec une autre substance, la mitoxantrone. Il participe également à une étude internationale pour évaluer le Campath (jusqu'ici essentiellement utilisé pour traiter la leucémie chronique) sur un échantillon plus large de patients.
« La vraie évolution, c'est de donner ces médicaments à un stade précoce, chez des patients qui souffrent d'une SEP agressive, dit-il. Les résultats sont très intéressants, mais il y a des risques d'effets secondaires. La mitoxantrone détruit les lymphocytes B. Le Campath attaque les lymphocytes T. Il y a eu des cas de purpura, de lymphome, d'atteinte du rein. Ce ne sont pas des traitements que l'on pourra proposer à tous les patients ».
Les études démontrent un bénéfice sur deux à trois ans. Plus loin, on ne sait pas. « Il n'y a pas d'études qui vont durer trente ans. Et attention, ces traitements ne guérissent pas la maladie. Ils contrôlent l'inflammation, mais ils sont puissants et toxiques. Le problème sera toujours de savoir quel est le rapport entre bénéfices et risques pour le patient. »
Philippe RICHARD.
mercredi 29 octobre 2008
Deux médicaments donnent des résultats deux fois plus efficaces pour contrôler l'évolution de la maladie. Mais ils sont très agressifs.
Une lueur d'espoir ? « Administré suffisamment tôt, le Campath pourrait efficacement stopper l'avancée de la maladie et rétablir des fonctions perdues en favorisant la reconstitution du tissu cérébral endommagé », assure le docteur Alastair Coles (Université de Cambridge).
La sclérose en plaques (SEP) est une maladie incurable du système nerveux, qui touche 80 000 personnes en France. Un dysfonctionnement du système immunitaire provoque la destruction de la myéline qui entoure les nerfs, conduisant à des handicaps plus ou moins lourds (baisse d'acuité visuelle, fatigue, troubles de l'humeur, paralysies partielles...).
L'étude britannique, publiée dans le New England Journal of Medicine, a porté sur 334 patients souffrant d'une forme agressive de la SEP à un stade précoce. Comparé au médicament de référence (Interféron beta-1a), le Campath a montré des résultats deux fois supérieurs. Pourtant, les précédents essais, sur des patients à des stades avancés de la maladie, avaient été des échecs.
Des résultats à Rennes
Au CHU de Rennes, le professeur Gilles Edan a contribué à une étude franco-italienne qui donne des résultats approchants, avec une autre substance, la mitoxantrone. Il participe également à une étude internationale pour évaluer le Campath (jusqu'ici essentiellement utilisé pour traiter la leucémie chronique) sur un échantillon plus large de patients.
« La vraie évolution, c'est de donner ces médicaments à un stade précoce, chez des patients qui souffrent d'une SEP agressive, dit-il. Les résultats sont très intéressants, mais il y a des risques d'effets secondaires. La mitoxantrone détruit les lymphocytes B. Le Campath attaque les lymphocytes T. Il y a eu des cas de purpura, de lymphome, d'atteinte du rein. Ce ne sont pas des traitements que l'on pourra proposer à tous les patients ».
Les études démontrent un bénéfice sur deux à trois ans. Plus loin, on ne sait pas. « Il n'y a pas d'études qui vont durer trente ans. Et attention, ces traitements ne guérissent pas la maladie. Ils contrôlent l'inflammation, mais ils sont puissants et toxiques. Le problème sera toujours de savoir quel est le rapport entre bénéfices et risques pour le patient. »
Philippe RICHARD.
Le gras animal montré du doigt
vendredi 31 octobre 2008 à 16 h 37
Les changements métaboliques induits par pareille alimentation affectent la réponse inflammatoire dans le cerveau, pensent les chercheurs. Cela expliquerait le lien qui existe entre la consommation de gras et l'alzheimer.
Les auteurs ne peuvent affirmer avec certitude que ce qu'ils ont observé chez les souris se produise aussi chez les humains, mais ils sont portés à croire qu'une alimentation contenant plus d'oméga-3 et moins de gras saturés préviendrait le développement de l'alzheimer, à tout le moins chez les gens qui ont des prédispositions génétiques à cette maladie.
Le détail de cette étude est publié dans la revue Neurobiology of Aging.
Le régime alimentaire dans les pays occidentaux serait-il directement lié à l'apparition de l'alzheimer?
Des chercheurs de l'Université Laval affirment que les principaux marqueurs neurologiques de cette maladie neurodégénérative sont accentués dans le cerveau de souris génétiquement prédisposées, lorsque leur alimentation est riche en gras animal et pauvre en acides gras oméga-3.
Leurs travaux
Une lignée de souris transgéniques qui manifestent deux symptômes observés chez les personnes qui souffrent d'alzheimer a été utilisée dans cette expérience.
Ces rongeurs produisent des protéines bêta-amyloïdes, associées à la formation des plaques séniles dans le cerveau des personnes atteintes d'alzheimer, et des protéines tau, qui altèrent les microtubules des neurones, produisant un enchevêtrement qui rend ces cellules non fonctionnelles.
Les chercheurs ont soumis ces souris et des souris normales à différents régimes alimentaires pendant neuf mois pour ensuite comparer leurs effets respectifs sur le cerveau des rongeurs.
Les souris dont l'alimentation était pauvre en oméga-3 et riche en gras affichaient des concentrations de protéines bêta-amyloïdes et de protéines tau respectivement 8,7 fois et 1,5 fois plus élevées que les souris du groupe témoin, dont la nourriture contenait sept fois moins de gras.
Le régime riche en gras a aussi provoqué une baisse de la protéine drébrine dans le cerveau, un autre phénomène associé à l'alzheimer.
Un faible apport en oméga-3 et surtout une forte proportion de calories consommées sous forme de graisses influencent l'évolution de ces trois marqueurs de l'alzheimer dans le cerveau des souris.
Les changements métaboliques induits par pareille alimentation affectent la réponse inflammatoire dans le cerveau, pensent les chercheurs. Cela expliquerait le lien qui existe entre la consommation de gras et l'alzheimer.
Les auteurs ne peuvent affirmer avec certitude que ce qu'ils ont observé chez les souris se produise aussi chez les humains, mais ils sont portés à croire qu'une alimentation contenant plus d'oméga-3 et moins de gras saturés préviendrait le développement de l'alzheimer, à tout le moins chez les gens qui ont des prédispositions génétiques à cette maladie.
Le détail de cette étude est publié dans la revue Neurobiology of Aging.
jeudi 23 octobre 2008
Un remède anti-leucémie stoppe et inverse les effets de la sclérose
AFP 23/10/2008
LONDRES (AFP) — Un médicament, développé à l'origine pour traiter la leucémie, peut stopper voire inverser les effets débilitants de la sclérose en plaques (SEP), ont annoncé des chercheurs de l'Université de Cambridge.
Au cours des essais, l'alemtuzumab a réduit le nombre d'attaques chez les malades et leur a aussi permis de récupérer des fonctions perdues, en permettant apparemment au tissu cérébral de se réparer, de sorte que des individus étaient moins handicapés à la fin qu'au début de l'étude, selon ces chercheurs.
"La possibilité qu'un traitement contre la SEP favorise la reconstitution du tissu cérébral est sans précédent", a affirmé le Dr Alasdair Coles, enseignant au département de neurosciences cliniques de Cambridge, qui a coordonné une partie de l'étude, publiée dans le New England Journal of Medecine.
"Nous sommes en présence d'un médicament qui, s'il est administré suffisamment tôt, pourrait efficacement stopper l'avancée de la maladie et également rétablir des fonctions perdues en favorisant la reconstitution du tissu cérébral endommagé", a-t-il expliqué.
La MS Society, la plus importante organisation caritative britannique consacrée au soutien des personnes atteintes de SEP, s'est dit "ravie" des résultats de l'étude.
"C'est le premier médicament qui a montré un potentiel pour arrêter et même inverser les effets débilitants de la SEP", s'est réjoui le chef de la recherche de la MS Society, Lee Dunster.
"Des travaux supplémentaires sont nécessaires pour prouver l'effet à long terme de ce traitement et nous attendons avec impatience les résultats de la prochaine étape - déjà en cours - de cette importante recherche", a-t-il poursuivi.
La SEP est une maladie incurable du système nerveux central qui touche 2,5 millions de personnes dans le monde.
Cette infection inflammatoire provoque la destruction de la myéline, une substance entourant les nerfs et assurant la transmission rapide de l'influx nerveux. Elle conduit à des handicaps plus ou moins lourds, notamment pertes de vision, de mobilité, troubles cognitifs.
L'étude sur trois ans a porté sur 334 patients souffrant d'une forme rémittente de SEP à un stade précoce qui n'avait pas été traité auparavant. Un groupe a reçu de l'alemtuzumab, un autre un médicament contre la SEP, l'interferon beta-1a.
L'alemtuzumab a permis une réduction plus importante que l'autre médicament du nombre d'attaques et du risque de handicaps durables.
Plusieurs individus du premier groupe ont également récupéré certaines fonctions perdues alors que les handicaps des patients du second groupe ont empiré, selon l'étude.
Leukemia drug improves multiple sclerosis symptoms in some people
Nathan Seppa
Web edition : Wednesday, October 22nd, 2008
A disease thought to be incurable is now a step closer to losing that dispiriting reputation. Multiple sclerosis, the disabling neuromuscular disease that has resisted effective drug therapy, eases off in some people given a drug normally prescribed for leukemia, researchers report in the Oct. 23 New England Journal of Medicine.
“More than half the patients in this study actually improved a significant amount” when taking the drug alemtuzumab, says study coauthor David Margolin, a neurologist at Genzyme Corp. in Cambridge, Mass., which teamed with an international team of researchers in conducting the trial. “We think this is something very special.”
That optimism is tempered by worrisome side effects that showed up in MS patients taking the drug. Two more large-scale trials of MS patients are now getting under way to address those issues and confirm the positive findings.
In MS, the body’s own immune cells orchestrate an attack on myelin, the fatty sheaths that insulate nerve fibers in the central nervous system. The origins of this mutiny remain a medical mystery, but the disaster that follows is well documented: A torrent of inflammation robs the nerves of their protective myelin, disrupting nerve signals and resulting in the motor control losses that mark MS. In the early stages, MS attacks often come and go in relapsing-and-remitting fashion. In the worst case scenario, the autoimmune assault becomes chronic, leading to irreparable nerve damage and permanent disability.
Enter alemtuzumab, also called Campath. This drug targets a compound called CD52, which appears on T cells and B cells, the prime movers of the immune system. Alemtuzumab works well, killing off nearly all the T and B cells, and thus wiping out a huge portion of a person’s immune system. That’s a good thing if your immune cells are running amok, as in autoimmune disease or leukemia. But it can leave a person vulnerable to infection.
Fortunately, this housecleaning is temporary. Since nascent T and B cells don’t make CD52, they escape the purge and go on to repopulate the immune system anew. That takes a few months for B cells but years for T cells, says study coauthor Alisdair Coles, a neurologist at the University of Cambridge in England.
While the drug has helped patients fight chronic lymphocytic leukemia, testing against MS progressed slowly in the 1990s as researchers mainly tested alemtuzumab in advanced-stage, mostly middle-aged MS patients, with little success.
That approach changed in 2002 when an international team of researchers began testing the drug on younger, less-advanced-stage MS patients over the course of a three-year trial. The scientists enrolled people mainly in their 20s and 30s with MS that was diagnosed only 1.3 years earlier, on average, and who hadn’t been treated for the condition yet.
The researchers randomly assigned 111 to get interferon beta 1a, a standard MS drug given as three injections per week. Another 223 patients received alemtuzumab, delivered in a series of intravenous infusions over five days once a year. Most volunteers getting alemtuzumab got two series of infusions, one at the outset and another after 12 months; 46 received a third course a year after that.
The interferon group was slated to receive regular injections during the three-year trial, but two-fifths stopped taking the drug at some point, most complaining of side effects or lack of effectiveness. All patients were monitored for three years.
Clinical testing showed that disabilities for people on interferon rose on average during the trial but fell in those getting alemtuzumab, a first for a large trial, the authors point out.
Overall, 57 percent of those on alemtuzumab improved during the study, while roughly one-fifth worsened and the others held steady. Of those getting interferon, one-third improved, 41 percent declined and the rest held even.
Over the three years, only 20 percent of the alemtuzumab patients had a relapse, compared with 48 percent of the interferon patients.
What’s more, magnetic resonance imaging, or MRI, of the patients’ brains showed less inflammation in those getting alemtuzumab. The brain can wither in MS patients. Between months 12 and 36 in this study, interferon patients experienced a slight loss of brain volume on average whereas alemtuzumab patients added volume.
Combined, these findings suggest that the drug is somehow promoting brain repair in MS patients. “This is unprecedented. It hasn’t been seen before,” says Coles. “Up until now, no one would have thought this would happen.” He was particularly surprised by the MRI data. “Between 12 and 36 months,” he says, patients getting alemtuzumab “were actually acquiring new tissue in the brain.”
The most common side effect from alemtuzumab concerns the thyroid gland, and 23 percent of patients getting the drug in this trial developed thyroid problems. In some people, the gland becomes overactive; in others, it became underactive. Of those getting inferferon, 3 percent developed thyroid problems.
Immunologist Bibiana Bielekova of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., says these thyroid problems are not always easy to treat. Plus, many patients with early-stage MS and mild symptoms might not relish the risk of developing a new problem, particularly when there are several other options available for treating their MS at that stage.
On the other hand, Margolin says, thyroid problems, if manageable, “might be a fair trade off” since they aren’t as serious as MS.
A dangerous bleeding disorder called ITP, or idiopathic thrombocytopenic purpura, showed up in 3 percent of alemtuzumab patients and 1 percent of interferon patients. ITP patients’ immune cells attack their own blood-clotting platelets, risking hemorrhage. One person on alemtuzumab died from the disorder.
“We are quite aware of how incredibly effective this drug is,” Bielekova says. “But everybody is scared to death of those side effects.”
Margolin says physicians will closely monitor patients’ platelet counts in the two upcoming trials of alemtuzumab.
Previous studies had gauged alemtuzumab’s effects against MS largely in patients who had late-stage disease. The drug showed promise, but patients still went downhill, Bielekova says.
Margolin suggests that using alemtuzumab to treat early-stage MS patients “who are still walking around” yields benefits because temporarily knocking out T cells and B cells quells the immune system’s ability to generate inflammation, an early-stage event in MS. “That seems to give the body a chance to recover,” he says.
The new findings are “remarkable,” says Stephen Hauser, a neurologist at the University of California, San Francisco, writing in the same NEJM issue. This and previous work pitting alemtuzumab against MS represent “thoughtful clinical investigations [that] have advanced the field substantially,” he says. But only long-term testing will establish alemtuzumab’s place in the anti-MS armamentarium, he says.
Web edition : Wednesday, October 22nd, 2008
A disease thought to be incurable is now a step closer to losing that dispiriting reputation. Multiple sclerosis, the disabling neuromuscular disease that has resisted effective drug therapy, eases off in some people given a drug normally prescribed for leukemia, researchers report in the Oct. 23 New England Journal of Medicine.
“More than half the patients in this study actually improved a significant amount” when taking the drug alemtuzumab, says study coauthor David Margolin, a neurologist at Genzyme Corp. in Cambridge, Mass., which teamed with an international team of researchers in conducting the trial. “We think this is something very special.”
That optimism is tempered by worrisome side effects that showed up in MS patients taking the drug. Two more large-scale trials of MS patients are now getting under way to address those issues and confirm the positive findings.
In MS, the body’s own immune cells orchestrate an attack on myelin, the fatty sheaths that insulate nerve fibers in the central nervous system. The origins of this mutiny remain a medical mystery, but the disaster that follows is well documented: A torrent of inflammation robs the nerves of their protective myelin, disrupting nerve signals and resulting in the motor control losses that mark MS. In the early stages, MS attacks often come and go in relapsing-and-remitting fashion. In the worst case scenario, the autoimmune assault becomes chronic, leading to irreparable nerve damage and permanent disability.
Enter alemtuzumab, also called Campath. This drug targets a compound called CD52, which appears on T cells and B cells, the prime movers of the immune system. Alemtuzumab works well, killing off nearly all the T and B cells, and thus wiping out a huge portion of a person’s immune system. That’s a good thing if your immune cells are running amok, as in autoimmune disease or leukemia. But it can leave a person vulnerable to infection.
Fortunately, this housecleaning is temporary. Since nascent T and B cells don’t make CD52, they escape the purge and go on to repopulate the immune system anew. That takes a few months for B cells but years for T cells, says study coauthor Alisdair Coles, a neurologist at the University of Cambridge in England.
While the drug has helped patients fight chronic lymphocytic leukemia, testing against MS progressed slowly in the 1990s as researchers mainly tested alemtuzumab in advanced-stage, mostly middle-aged MS patients, with little success.
That approach changed in 2002 when an international team of researchers began testing the drug on younger, less-advanced-stage MS patients over the course of a three-year trial. The scientists enrolled people mainly in their 20s and 30s with MS that was diagnosed only 1.3 years earlier, on average, and who hadn’t been treated for the condition yet.
The researchers randomly assigned 111 to get interferon beta 1a, a standard MS drug given as three injections per week. Another 223 patients received alemtuzumab, delivered in a series of intravenous infusions over five days once a year. Most volunteers getting alemtuzumab got two series of infusions, one at the outset and another after 12 months; 46 received a third course a year after that.
The interferon group was slated to receive regular injections during the three-year trial, but two-fifths stopped taking the drug at some point, most complaining of side effects or lack of effectiveness. All patients were monitored for three years.
Clinical testing showed that disabilities for people on interferon rose on average during the trial but fell in those getting alemtuzumab, a first for a large trial, the authors point out.
Overall, 57 percent of those on alemtuzumab improved during the study, while roughly one-fifth worsened and the others held steady. Of those getting interferon, one-third improved, 41 percent declined and the rest held even.
Over the three years, only 20 percent of the alemtuzumab patients had a relapse, compared with 48 percent of the interferon patients.
What’s more, magnetic resonance imaging, or MRI, of the patients’ brains showed less inflammation in those getting alemtuzumab. The brain can wither in MS patients. Between months 12 and 36 in this study, interferon patients experienced a slight loss of brain volume on average whereas alemtuzumab patients added volume.
Combined, these findings suggest that the drug is somehow promoting brain repair in MS patients. “This is unprecedented. It hasn’t been seen before,” says Coles. “Up until now, no one would have thought this would happen.” He was particularly surprised by the MRI data. “Between 12 and 36 months,” he says, patients getting alemtuzumab “were actually acquiring new tissue in the brain.”
The most common side effect from alemtuzumab concerns the thyroid gland, and 23 percent of patients getting the drug in this trial developed thyroid problems. In some people, the gland becomes overactive; in others, it became underactive. Of those getting inferferon, 3 percent developed thyroid problems.
Immunologist Bibiana Bielekova of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., says these thyroid problems are not always easy to treat. Plus, many patients with early-stage MS and mild symptoms might not relish the risk of developing a new problem, particularly when there are several other options available for treating their MS at that stage.
On the other hand, Margolin says, thyroid problems, if manageable, “might be a fair trade off” since they aren’t as serious as MS.
A dangerous bleeding disorder called ITP, or idiopathic thrombocytopenic purpura, showed up in 3 percent of alemtuzumab patients and 1 percent of interferon patients. ITP patients’ immune cells attack their own blood-clotting platelets, risking hemorrhage. One person on alemtuzumab died from the disorder.
“We are quite aware of how incredibly effective this drug is,” Bielekova says. “But everybody is scared to death of those side effects.”
Margolin says physicians will closely monitor patients’ platelet counts in the two upcoming trials of alemtuzumab.
Previous studies had gauged alemtuzumab’s effects against MS largely in patients who had late-stage disease. The drug showed promise, but patients still went downhill, Bielekova says.
Margolin suggests that using alemtuzumab to treat early-stage MS patients “who are still walking around” yields benefits because temporarily knocking out T cells and B cells quells the immune system’s ability to generate inflammation, an early-stage event in MS. “That seems to give the body a chance to recover,” he says.
The new findings are “remarkable,” says Stephen Hauser, a neurologist at the University of California, San Francisco, writing in the same NEJM issue. This and previous work pitting alemtuzumab against MS represent “thoughtful clinical investigations [that] have advanced the field substantially,” he says. But only long-term testing will establish alemtuzumab’s place in the anti-MS armamentarium, he says.
mercredi 15 octobre 2008
Response To Immune Protein Determines Pathology Of Multiple Sclerosis
Science Daily
Mon, 13 Oct 2008
New research may help reveal why different parts of the brain can come under attack in patients with multiple sclerosis (MS). According to a new study in mice with an MS-like disease, the brain's response to a protein produced by invading T cells dictates whether it's the spinal cord or cerebellum that comes under fire.
The study - from researchers at the University of Maryland School of Medicine in Baltimore and Washington University in St. Louis - will be published online on October 13th in the Journal of Experimental Medicine.
In most MS patients, the disease primarily affects the spinal cord and the white matter of the brain. But a small percentage of patients develop an atypical form of the disease, which primarily affects the cerebellum - the part of the brain that controls sensory perception and movement. For these patients, the disease tends to progress more rapidly and the prognosis is particularly bleak.
MS ensues when the body's T cells invade the brain and trigger nerve-damaging inflammation, in part by secreting proteins called cytokines. According to the new study, lead by Washington University scientist John Russell, the brain's response to one particular immune protein, called interferon-g (IFNg), determines which part of the brain the T cells attack. In mice that are oblivious to IFNg (because they lack its receptor), mice suffer cerebellum and brain stem inflammation, but their spinal cords are spared. When IFNg receptors were left intact, the reverse occurred.
Exactly how the brain's response to IFNg directs the T cell attack is not yet known, but the authors suspect that IFNg triggers a localized production of T cell-attracting proteins in the spinal cord. Translating the details of the "conversation" between T cells and brain cells, suggests Russell, might bring scientists closer to understanding the variable manifestations of human MS.
Mon, 13 Oct 2008
New research may help reveal why different parts of the brain can come under attack in patients with multiple sclerosis (MS). According to a new study in mice with an MS-like disease, the brain's response to a protein produced by invading T cells dictates whether it's the spinal cord or cerebellum that comes under fire.
The study - from researchers at the University of Maryland School of Medicine in Baltimore and Washington University in St. Louis - will be published online on October 13th in the Journal of Experimental Medicine.
In most MS patients, the disease primarily affects the spinal cord and the white matter of the brain. But a small percentage of patients develop an atypical form of the disease, which primarily affects the cerebellum - the part of the brain that controls sensory perception and movement. For these patients, the disease tends to progress more rapidly and the prognosis is particularly bleak.
MS ensues when the body's T cells invade the brain and trigger nerve-damaging inflammation, in part by secreting proteins called cytokines. According to the new study, lead by Washington University scientist John Russell, the brain's response to one particular immune protein, called interferon-g (IFNg), determines which part of the brain the T cells attack. In mice that are oblivious to IFNg (because they lack its receptor), mice suffer cerebellum and brain stem inflammation, but their spinal cords are spared. When IFNg receptors were left intact, the reverse occurred.
Exactly how the brain's response to IFNg directs the T cell attack is not yet known, but the authors suspect that IFNg triggers a localized production of T cell-attracting proteins in the spinal cord. Translating the details of the "conversation" between T cells and brain cells, suggests Russell, might bring scientists closer to understanding the variable manifestations of human MS.
Inscription à :
Commentaires (Atom)
Articles
