John von Radowitz
The Independent
Mon, 09 Mar 2009
Disabling strokes could one day be treated by replacing damaged brain tissue with stem cells, scientists have shown.
Researchers used a new technique to insert therapeutic stem cells into the brains of rats with pinpoint accuracy.
Once implanted the cells began to form new brain tissue and nerve connections.
The work is at an early stage and does not yet prove that stroke symptoms such as paralysis can be reversed.
But it demonstrates that lost brain tissue can be replaced with stem cells targeted at sites of damage.
Stem cells are immature cells with the ability to take on any of a number of specialist roles.
In previous animal experiments, stem cells implanted into the brain have tended to migrate to surrounding healthy tissue rather than fill up the hole left by a stroke.
Scientists from King's College London and the University of Nottingham overcame the problem by loading the cells onto biodegradable particles.
These were then injected through a fine needle to the precise site of damage, located using a magnetic resonance imaging (MRI) scanner.
Once implanted, the particles disappeared leaving gaps for the growth of new tissue and nourishing blood vessels.
The cells, derived from stem cells taken from mouse embryos, had already progressed some of the way to becoming neurons.
They were attached to particles made from a biodegradable plastic-like polymer called PLGA.
Dr Mike Modo, leading the King's College team from the university's Institute of Psychiatry, said: "The stem cell-loaded PLGA particles can be injected through a very fine needle and then adopt the precise shape of the cavity. In this process the cells fill the cavity and can make connections with other cells, which helps to establish the tissue.
"Over a few days we can see cells migrating along the scaffold particles and forming a primitive brain tissue that interacts with the host brain. Gradually the particles biodegrade leaving more gaps and conduits for tissue, fibres and blood vessels to move into."
Colleague Kevin Shakesheff, Professor of Advanced Drug Delivery and Tissue Engineering at the University of Nottingham, said: "This was a great collaborative project with the Kings College team and hopefully this technology will be taken to the clinical setting soon. Repairing damaged brain tissue is one of the ultimate challenges in medicine and science. It is great that we are now one step closer to achieving that goal."
The next stage will be to apply a "growth factor" chemical called VEGF with the particles to encourage the creation of new blood vessels.
The research, funded by the Biotechnology and Biological Sciences Research Council (BBSRC), is reported in the journal Biomaterials.
Strokes occur when part of the brain dies off because of a blocked or burst blood vessel.
An estimated 150,000 strokes occur in the UK each year, 67,000 of which are fatal.
Strokes cause more disability than any other chronic condition. Around 300,000 people in the UK are moderately or severely disabled because of a stroke.
Joe Korner, from the Stroke Association charity, said: "This research is another step towards using stem cell therapy in treating and reversing the brain damage caused by stroke. It is exciting because researchers have shown they are able to overcome some of the many challenges in translating the potential of using stem cells into reality.
"The potential to reverse the disabling effects of stroke seems to have been proved. However the development of stem cell therapy for stroke survivors is still in the early stages and much more research will be needed before it can be tested in humans or used in practice.
"Every five minutes someone in the UK has a stroke and it is vital that we do all we can to help those affected by stroke."
Professor Douglas Kell, chief executive of the BBSRC, said: "Stroke is a leading cause of disability in industrialised countries. It is reassuring to know that the technology for treating stroke by repairing brain damage is getting ever closer to translation into the clinic. This crucial groundwork by Dr Modo and his colleagues will surely be a solid foundation of basic research for much better treatments in the future."
Anthony Hollander, Professor of Rheumatology and Tissue Engineering at the University of Bristol, said: "We are only just beginning to understand how to use tissue engineering to cure diseases. This study shows the exciting possibility of using a biomaterial to deliver stem cells to a very specific location in the brain. It is too early to say if it will be clinically effective in patients but the more we explore these possibilities the more likely it is that we will develop successful therapies."
lundi 9 mars 2009
mardi 3 mars 2009
Two distinct molecular pathways can make regulatory immune cells
Finding a way to bypass the molecular events involved in autoimmunity - where the body's immune system mounts a self-directed attack - could lead to new treatments for autoimmune disorders and chronic infections. A study published in this week's issue of PLoS Biology describes genetic evidence that two distinct molecular pathways control the formation of regulatory T cells (Treg), a cell type vitally important in limiting undesirable immune responses.
Treg cells are like the peace-keepers of the immune defence system - they limit the actions of effector T cells, the foot-soldiers of the body. If the body lacks sufficient numbers of Treg cells, it loses the ability to tone down immune responses once invading pathogens are cleared. In addition, the body is unable to suppress T cell responses that recognize and target the body itself. The latter can lead to autoimmunity, which can destroy vital tissues and organs.
Under normal healthy conditions, the majority of Treg cells are derived from an organ called the thymus. New work from researchers at Cincinnati Children's Hospital Medical Center and The Scripps Research Institute in California, shows that if a gene called Carma1 isn't expressed normally, Treg development is impaired in the thymus. Mutations in Carma1 can result in a failure of the thymus to produce Treg cells, said senior investigator Kasper Hoebe, Ph.D., a researcher at Cincinnati.
But the study also points to a second molecular pathway - occurring in the peripheral lymphoid system - that is known to result in development of Treg cells. This means if the process in the thymus breaks down, as in the case with Carma1 mutations, Treg cells created in the peripheral lymphoid system can compensate.
"We show that the two pathways for Treg development are molecularly distinct, and Treg can arise quite well in the peripheral lymphoid system, via mechanisms that are independent of the thymic process," Dr. Hoebe said. "This is important because it shows the flexibility of the immune system to regulate T cell responses. If we understand the molecular requirements of these pathways we can potentially use these as targets for therapeutic intervention - which is the eventual goal."
Possible therapies may include the ability to repress the self-destructive immune response in autoimmune disease by increasing Treg development, or achieving the opposite effect to treat chronic infectious diseases - inhibiting Treg development and promoting activation of destructive T cells.
More information: Barnes MJ, Krebs P, Harris N, Eidenschenk C, Gonzalez-Quintial R, et al. (2009) Commitment to the regulatory T cell lineage requires CARMA1 in the thymus but not in the periphery. PLoS Biol 7(3): e1000051. doi:10.1371/journal.pbio.1000051, http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.1000051
Source: Public Library of Science
Treg cells are like the peace-keepers of the immune defence system - they limit the actions of effector T cells, the foot-soldiers of the body. If the body lacks sufficient numbers of Treg cells, it loses the ability to tone down immune responses once invading pathogens are cleared. In addition, the body is unable to suppress T cell responses that recognize and target the body itself. The latter can lead to autoimmunity, which can destroy vital tissues and organs.
Under normal healthy conditions, the majority of Treg cells are derived from an organ called the thymus. New work from researchers at Cincinnati Children's Hospital Medical Center and The Scripps Research Institute in California, shows that if a gene called Carma1 isn't expressed normally, Treg development is impaired in the thymus. Mutations in Carma1 can result in a failure of the thymus to produce Treg cells, said senior investigator Kasper Hoebe, Ph.D., a researcher at Cincinnati.
But the study also points to a second molecular pathway - occurring in the peripheral lymphoid system - that is known to result in development of Treg cells. This means if the process in the thymus breaks down, as in the case with Carma1 mutations, Treg cells created in the peripheral lymphoid system can compensate.
"We show that the two pathways for Treg development are molecularly distinct, and Treg can arise quite well in the peripheral lymphoid system, via mechanisms that are independent of the thymic process," Dr. Hoebe said. "This is important because it shows the flexibility of the immune system to regulate T cell responses. If we understand the molecular requirements of these pathways we can potentially use these as targets for therapeutic intervention - which is the eventual goal."
Possible therapies may include the ability to repress the self-destructive immune response in autoimmune disease by increasing Treg development, or achieving the opposite effect to treat chronic infectious diseases - inhibiting Treg development and promoting activation of destructive T cells.
More information: Barnes MJ, Krebs P, Harris N, Eidenschenk C, Gonzalez-Quintial R, et al. (2009) Commitment to the regulatory T cell lineage requires CARMA1 in the thymus but not in the periphery. PLoS Biol 7(3): e1000051. doi:10.1371/journal.pbio.1000051, http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.1000051
Source: Public Library of Science
samedi 28 février 2009
Un médicament améliore la marche de patients atteints de sclérose en plaques
PARIS (AFP) — Un médicament améliore la marche chez des malades atteints de sclérose en plaques et semble bien toléré, selon les résultats d'un essai clinique sur 300 personnes publiés vendredi dans la revue médicale The Lancet.
L'essai clinique de phase III (dernière étape avant la demande de mise sur le marché) a été conduit par Andrew Goodman (université de Rochester, New York) et ses collègues dans 33 centres de lutte contre la sclérose en plaques (SEP) aux Etats-Unis et au Canada.
301 personnes atteintes de SEP, âgées entre 18 et 70 ans, ont reçu pendant 14 semaines soit le médicament fampridine (10 mg deux fois par jour), soit un placebo.
La proportion des malades dont la vitesse de marche s'est améliorée était nettement supérieure dans le groupe traité avec la fampridine (35%) que dans le groupe témoin ayant reçu le placebo (8%), selon les résultats de cet essai.
La SEP, maladie neurologique particulièrement invalidante, provoque une dégradation de la gaine de myéline qui protège les fibres nerveuses (cerveau, moelle épinière et nerf optique), ce qui ralentit la vitesse de conduction de l'influx nerveux.
Cette maladie chronique, qui touche le plus souvent le jeune adulte, concerne quelque 80.000 personnes en France et 350.000 en Europe.
La fampridine n'agit pas sur le processus de démyélinisation mais contribue à améliorer la transmission de l'influx nerveux.
La société Acorda Therapeutics, qui a développé ce traitement, a déposé ce mois-ci une demande d'autorisation de mise sur le marché auprès de l'Agence américaine des médicaments (FDA).
Obtention de cellules souches neuronales
Des chercheurs de l'Université (Une université est un établissement d'enseignement supérieur dont l'objectif est la production du savoir (recherche),...) de Bonn ont réussi à obtenir des cellules souches neuronales à partir de cellules souches embryonnaires humaines.
Ces cellules présentent l'intérêt non seulement de pouvoir se conserver presque sans limite dans une culture (La définition que donne l'UNESCO de la culture est la suivante [1] :), mais également de servir de source presque inépuisable pour différents types de cellules nerveuses. Cette recherche (La recherche scientifique désigne en premier lieu l’ensemble des actions entreprises en vue de produire et de...) a aussi permis de démontrer que ces cellules nerveuses peuvent s'intégrer dans les circuits neuronaux du cerveau.
L'étude est publiée dans la prochaine édition de Proceedings of the National Academy of Sciences PNAS (doi: 10.1073/pnas.0808387106).
Pendant des années, la recherche sur les cellules souches a semblé divisée en deux mondes: les cellules sources embryonnaires au développement illimité d'une part, et les cellules souches somatiques qui peuvent être obtenues à partir de tissus d'adultes, mais ces dernières cellules étaient limitées dans leur potentiel de développement.
Les scientifiques de l'Université de Bonn ont rapproché ces deux mondes en créant des cellules souches du cerveau pouvant se multiplier et se conserver quasiment indéfiniment. C'est à partir de ces cellules que les chercheurs ont pu obtenir différentes cellules nerveuses dont des semblables à celles observées dans la maladie de Parkinson.
L'expérimentation sur des animaux a prouvé que ces cellules nerveuses obtenues artificiellement fonctionnaient bien. Les cellules transplantées sur des souris de laboratoire sont entrées en contact avec le cerveau du receveur pouvant émettre des signaux et en recevoir. Les chercheurs veulent utiliser cette source quasi inépuisable de cellules nerveuses humaines pour faire des études sur les maladies neuro-dégénératives.
Source: communiqué de presse de l'Université de Bonn
Illustration: Wikipédia
Ces cellules présentent l'intérêt non seulement de pouvoir se conserver presque sans limite dans une culture (La définition que donne l'UNESCO de la culture est la suivante [1] :), mais également de servir de source presque inépuisable pour différents types de cellules nerveuses. Cette recherche (La recherche scientifique désigne en premier lieu l’ensemble des actions entreprises en vue de produire et de...) a aussi permis de démontrer que ces cellules nerveuses peuvent s'intégrer dans les circuits neuronaux du cerveau.
L'étude est publiée dans la prochaine édition de Proceedings of the National Academy of Sciences PNAS (doi: 10.1073/pnas.0808387106).
Pendant des années, la recherche sur les cellules souches a semblé divisée en deux mondes: les cellules sources embryonnaires au développement illimité d'une part, et les cellules souches somatiques qui peuvent être obtenues à partir de tissus d'adultes, mais ces dernières cellules étaient limitées dans leur potentiel de développement.
Les scientifiques de l'Université de Bonn ont rapproché ces deux mondes en créant des cellules souches du cerveau pouvant se multiplier et se conserver quasiment indéfiniment. C'est à partir de ces cellules que les chercheurs ont pu obtenir différentes cellules nerveuses dont des semblables à celles observées dans la maladie de Parkinson.
L'expérimentation sur des animaux a prouvé que ces cellules nerveuses obtenues artificiellement fonctionnaient bien. Les cellules transplantées sur des souris de laboratoire sont entrées en contact avec le cerveau du receveur pouvant émettre des signaux et en recevoir. Les chercheurs veulent utiliser cette source quasi inépuisable de cellules nerveuses humaines pour faire des études sur les maladies neuro-dégénératives.
Source: communiqué de presse de l'Université de Bonn
Illustration: Wikipédia
jeudi 5 février 2009
Les cellules souches montrent leurs effets contre la sclérose en plaques
MaxiScience
2009-02-05
États-Unis - Un essai clinique mené par une équipe de l’université de Chicago montre que l'état des malades atteints de sclérose en plaques s'améliore après une autogreffe de cellules souches.
Vingt-et-un malades ont été transplantés avec leurs propres cellules souches extraites de leur moelle osseuse, après destruction de la moelle par immunosuppresseurs. Le système immunitaire est ainsi « remis à zéro ». Trois ans après cette transplantation, tous les malades n’ont pas connu d’aggravation de la maladie et dix-sept ont vu leur handicap réduire.
La sclérose en plaques est une affection neurologique grave qui pousse le système immunitaire à attaquer la myéline, couche protectrice des fibres nerveuses. Les inflammations sont constatées au niveau du cerveau, dans la moelle épinière et les nerfs. La sclérose en plaques évolue par poussées qui laissent des séquelles lourdes comme des troubles moteurs, des troubles de la coordination, des vertiges ou des problèmes de vue.
Aux différents stades de la maladie, des solutions chimiques existent. Cet essai a été réalisé sur des personnes trentenaires au premier stade de la maladie. Cette technique lourde de traitement ne sera pas applicable à tous les malades.
2009-02-05
États-Unis - Un essai clinique mené par une équipe de l’université de Chicago montre que l'état des malades atteints de sclérose en plaques s'améliore après une autogreffe de cellules souches.
Vingt-et-un malades ont été transplantés avec leurs propres cellules souches extraites de leur moelle osseuse, après destruction de la moelle par immunosuppresseurs. Le système immunitaire est ainsi « remis à zéro ». Trois ans après cette transplantation, tous les malades n’ont pas connu d’aggravation de la maladie et dix-sept ont vu leur handicap réduire.
La sclérose en plaques est une affection neurologique grave qui pousse le système immunitaire à attaquer la myéline, couche protectrice des fibres nerveuses. Les inflammations sont constatées au niveau du cerveau, dans la moelle épinière et les nerfs. La sclérose en plaques évolue par poussées qui laissent des séquelles lourdes comme des troubles moteurs, des troubles de la coordination, des vertiges ou des problèmes de vue.
Aux différents stades de la maladie, des solutions chimiques existent. Cet essai a été réalisé sur des personnes trentenaires au premier stade de la maladie. Cette technique lourde de traitement ne sera pas applicable à tous les malades.
La vitamine D pourrait prévenir la sclérose en plaques
PsychoMédia
05 février 2009
Une interaction directe entre la vitamine D et une variation génétique associée à la sclérose en plaques (SEP) modifie le risque de développer la maladie selon une récente étude publiée dans PLoS Genetics. L'étude suggère qu'une carence en vitamine D pendant la grossesse et durant les premières années pourrait augmenter le risque de développer la SEP plus tard dans la vie, considèrent les chercheurs.
La SEP est l'affection neurologique la plus fréquente chez les jeunes adules. Des facteurs génétiques et environnementaux sont à l'origine de la maladie.
Des études précédentes avaient montré que les populations des pays de l'Europe du Nord ont un risque plus élevé de SEP s'ils habitent dans des régions moins ensoleillées. Ce qui suggère un lien direct entre une carence en vitamine D, qui est produite par l'organisme en réponse à l'action de la lumière du soleil sur la peau, et un risque accru de SEP.
Le facteur génétique qui est de loin le plus important est la variation DRB1*1501, située sur le chromosome 6, et les séquences ADN adjacentes.
Des chercheurs de l'Université d'Oxford et de l'Université Columbia ont montré que des protéines activées par la vitamine D se lient à une séquence particulière de l'ADN qui se situe près de la variation DRB1*1501 et activent le gène.
"Chez les personnes qui portent la variation DRB1 associée à la sclérose en plaques, il semble que la vitamine D puisse joue un rôle critique", dit Dr Julian Knight, coauteur. "Si trop peu de vitamine est disponible, il est possible que le gène ne puisse pas fonctionner correctement". Ce gène agit sur le système immunitaire (rappelons que la SEP est une maladie auto-immune).
Cette étude suggère que de prendre des compléments de vitamine D durant la grossesse et durant les premières années pourrait réduire le risque de développer la SEP plus tard dans la vie", selon Dr Sreeram Ramagopalan qui a dirigé la recherche. (Il est difficile de combler les besoins en vitamine D par l'alimentation).
Psychomédia avec source:
Science Daily
05 février 2009
Une interaction directe entre la vitamine D et une variation génétique associée à la sclérose en plaques (SEP) modifie le risque de développer la maladie selon une récente étude publiée dans PLoS Genetics. L'étude suggère qu'une carence en vitamine D pendant la grossesse et durant les premières années pourrait augmenter le risque de développer la SEP plus tard dans la vie, considèrent les chercheurs.
La SEP est l'affection neurologique la plus fréquente chez les jeunes adules. Des facteurs génétiques et environnementaux sont à l'origine de la maladie.
Des études précédentes avaient montré que les populations des pays de l'Europe du Nord ont un risque plus élevé de SEP s'ils habitent dans des régions moins ensoleillées. Ce qui suggère un lien direct entre une carence en vitamine D, qui est produite par l'organisme en réponse à l'action de la lumière du soleil sur la peau, et un risque accru de SEP.
Le facteur génétique qui est de loin le plus important est la variation DRB1*1501, située sur le chromosome 6, et les séquences ADN adjacentes.
Des chercheurs de l'Université d'Oxford et de l'Université Columbia ont montré que des protéines activées par la vitamine D se lient à une séquence particulière de l'ADN qui se situe près de la variation DRB1*1501 et activent le gène.
"Chez les personnes qui portent la variation DRB1 associée à la sclérose en plaques, il semble que la vitamine D puisse joue un rôle critique", dit Dr Julian Knight, coauteur. "Si trop peu de vitamine est disponible, il est possible que le gène ne puisse pas fonctionner correctement". Ce gène agit sur le système immunitaire (rappelons que la SEP est une maladie auto-immune).
Cette étude suggère que de prendre des compléments de vitamine D durant la grossesse et durant les premières années pourrait réduire le risque de développer la SEP plus tard dans la vie", selon Dr Sreeram Ramagopalan qui a dirigé la recherche. (Il est difficile de combler les besoins en vitamine D par l'alimentation).
Psychomédia avec source:
Science Daily
Vitamin D is ray of sunshine for multiple sclerosis patients
Melanie Reid and Oliver Gillie
Times Online
Thu, 05 Feb 2009
Multiple sclerosis could be prevented through daily vitamin D supplements, scientists told The Times last night.
The first causal link has been established between the "sunshine vitamin" and a gene that increases the risk of MS, raising the possibility that the debilitating auto-immune disease could be eradicated.
George Ebers, Professor of Clinical Neurology at the University of Oxford, claimed that there was hard evidence directly relating both genes and the environment to the origins of MS.
His work suggests that vitamin D deficiency during pregnancy and childhood may increase the risk of a child developing the diease.
He has also established the possibility that genetic vulnerability to MS, apparently initiated by lack of vitamin D, may be passed through families.
These risks might plausibly be reduced by giving vitamin D supplements to pregnant woman and young children.
"I think it offers the potential for treatment which might prevent MS in the future," Professor Ebers said.
"Our research has married two key pieces of the puzzle. The interaction of vitamin D with the gene is very specific and it seems most unlikely to be a coincidence of any kind."
Warnings over sun exposure could now also be called into question - sunlight allows the body to produce the vitamin.
Professor Ebers said: "Serious questions now arise over the wisdom of current advice to limit sun exposure and avoid sunbathing. We also need to give better advice and help to the public on vitamin D supplements, particularly pregnant and nursing mothers."
The news has momentous implications for Scotland and other northern countries, where the incidence of multiple sclerosis is the highest in the world. It will give added urgency to recent moves by Scotland's Chief Medical Officer to consider recommending vitamin D supplements.
Deficiency in vitamin D, caused by lack of exposure to sunshine, has been increasingly linked to the cloudier climate in Scotland and other northern latitudes. The deficiency is twice as common among the Scots as it is amongst the English - and Orkney and Shetland have among the highest rates.
Studies have also shown that fewer people with MS are born in November and more in May, implicating a lack of sunshine during pregnancy.
The breakthrough comes after a groundswell of expert belief in the importance of vitamin D. Last November, at a conference organised by the Scottish Government, international experts urged vitamin D supplements for Scots to be tested "sooner rather than later" to find whether they could improve the nation's health.
Researchers for the World Health Organisation said there should be large, randomised trials as there was strong evidence that increased daily intake of vitamin D could significantly improve health.
The seminar followed evidence, revealed in The Times, that Scotland's poor health record has close links to vitamin D deficiency. Last September this newspaper reported evidence from scientists in Canada that children with early symptoms of multiple sclerosis have low levels of vitamin D.
Until now there has been no scientific proof of the links. However, Professor Ebers and his team have shown that vitamin D affects a particular genetic variant, identified as the one that increases the risk of developing MS threefold.
They suggest that a shortage of the vitamin alters this variant, thus preventing the immune system from functioning normally.
Professor Ebers said: "Whether it's at the core of MS is going to take some further work, but it does look like a reasonably good chance."
Last October Professor Ebers, in an article in The Times, backed the idea of distributing vitamin D supplements in Scotland to guard against conditions that may be linked to a deficiency, including MS.
"It is plausible that some 200 cases a year of MS might be prevented in Scotland alone by giving vitamin D to mothers and children," he wrote.
"Over a trial duration of 25 years, 5,000 cases of this disease might be otherwise prevented.
"The economic impact of each person with MS is at least an extra million pounds during a lifetime.
"Over 25 years £5 billion is at issue in this disease without factoring in the human cost, the increasing rate of MS or inflation. A large-scale programme providing vitamin D could provide scientific evidence."
Disease of the North: MS rates per 100,000 of the population
Canada 240
Scotland 150 - 200
Norway 110
England and Wales 90 - 110
Australia 78
Spain 59
Brazil 18
Sources: Atlas of Multiple Sclerosis
Times Online
Thu, 05 Feb 2009
Multiple sclerosis could be prevented through daily vitamin D supplements, scientists told The Times last night.
The first causal link has been established between the "sunshine vitamin" and a gene that increases the risk of MS, raising the possibility that the debilitating auto-immune disease could be eradicated.
George Ebers, Professor of Clinical Neurology at the University of Oxford, claimed that there was hard evidence directly relating both genes and the environment to the origins of MS.
His work suggests that vitamin D deficiency during pregnancy and childhood may increase the risk of a child developing the diease.
He has also established the possibility that genetic vulnerability to MS, apparently initiated by lack of vitamin D, may be passed through families.
These risks might plausibly be reduced by giving vitamin D supplements to pregnant woman and young children.
"I think it offers the potential for treatment which might prevent MS in the future," Professor Ebers said.
"Our research has married two key pieces of the puzzle. The interaction of vitamin D with the gene is very specific and it seems most unlikely to be a coincidence of any kind."
Warnings over sun exposure could now also be called into question - sunlight allows the body to produce the vitamin.
Professor Ebers said: "Serious questions now arise over the wisdom of current advice to limit sun exposure and avoid sunbathing. We also need to give better advice and help to the public on vitamin D supplements, particularly pregnant and nursing mothers."
The news has momentous implications for Scotland and other northern countries, where the incidence of multiple sclerosis is the highest in the world. It will give added urgency to recent moves by Scotland's Chief Medical Officer to consider recommending vitamin D supplements.
Deficiency in vitamin D, caused by lack of exposure to sunshine, has been increasingly linked to the cloudier climate in Scotland and other northern latitudes. The deficiency is twice as common among the Scots as it is amongst the English - and Orkney and Shetland have among the highest rates.
Studies have also shown that fewer people with MS are born in November and more in May, implicating a lack of sunshine during pregnancy.
The breakthrough comes after a groundswell of expert belief in the importance of vitamin D. Last November, at a conference organised by the Scottish Government, international experts urged vitamin D supplements for Scots to be tested "sooner rather than later" to find whether they could improve the nation's health.
Researchers for the World Health Organisation said there should be large, randomised trials as there was strong evidence that increased daily intake of vitamin D could significantly improve health.
The seminar followed evidence, revealed in The Times, that Scotland's poor health record has close links to vitamin D deficiency. Last September this newspaper reported evidence from scientists in Canada that children with early symptoms of multiple sclerosis have low levels of vitamin D.
Until now there has been no scientific proof of the links. However, Professor Ebers and his team have shown that vitamin D affects a particular genetic variant, identified as the one that increases the risk of developing MS threefold.
They suggest that a shortage of the vitamin alters this variant, thus preventing the immune system from functioning normally.
Professor Ebers said: "Whether it's at the core of MS is going to take some further work, but it does look like a reasonably good chance."
Last October Professor Ebers, in an article in The Times, backed the idea of distributing vitamin D supplements in Scotland to guard against conditions that may be linked to a deficiency, including MS.
"It is plausible that some 200 cases a year of MS might be prevented in Scotland alone by giving vitamin D to mothers and children," he wrote.
"Over a trial duration of 25 years, 5,000 cases of this disease might be otherwise prevented.
"The economic impact of each person with MS is at least an extra million pounds during a lifetime.
"Over 25 years £5 billion is at issue in this disease without factoring in the human cost, the increasing rate of MS or inflation. A large-scale programme providing vitamin D could provide scientific evidence."
Disease of the North: MS rates per 100,000 of the population
Canada 240
Scotland 150 - 200
Norway 110
England and Wales 90 - 110
Australia 78
Spain 59
Brazil 18
Sources: Atlas of Multiple Sclerosis
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