Category: Multiple Sclerosis

 A clinical study of 30 adult patients with multiple sclerosis (MS) at the University of California, San Diego School of Medicine has shown that smoked cannabis may be an effective treatment for spasticity — a common and disabling symptom of this neurological disease.

The placebo-controlled trial also resulted in reduced perception of pain, although participants also reported short-term, adverse cognitive effects and increased fatigue. The study will be published in the Canadian Medical Association Journal on May 14.

Principal investigator Jody Corey-Bloom, MD, PhD, professor of neurosciences and director of the Multiple Sclerosis Center at UC San Diego, and colleagues randomly assigned participants to either the intervention group (which smoked cannabis once daily for three days) or the control group (which smoked identical placebo cigarettes, also once a day for three days). After an 11-day interval, the participants crossed over to the other group.

"We found that smoked cannabis was superior to placebo in reducing symptoms and pain in patients with treatment-resistant spasticity, or excessive muscle contractions," said Corey-Bloom.

Earlier reports suggested that the active compounds of medical marijuana were potentially effective in treating neurologic conditions, but most studies focused on orally administered cannabinoids. There were also anecdotal reports of MS patients that endorsed smoking marijuana to relieve symptoms of spasticity.

However, this trial used a more objective measurement, a modified Ashford scale which graded the intensity of muscle tone by measuring such things as resistance in range of motion and rigidity. The secondary outcome, pain, was measured using a visual analogue scale. The researchers also looked at physical performance (using a timed walk) and cognitive function and — at the end of each visit — asked patients to assess their feeling of "highness."

Although generally well tolerated, smoking cannabis did have mild effects on attention and concentration. The researchers noted that larger, long-terms studies are needed to confirm their findings and determine whether lower doses can result in beneficial effects with less cognitive impact.

The current study is the fifth clinical test of the possible efficacy of cannabis for clinical use reported by the University of California Center for Medicinal Cannabis Research (CMCR). Four other human studies on control of neuropathic pain also reported positive results.

"The study by Corey Bloom and her colleagues adds to a growing body of evidence that cannabis has therapeutic value for selected indications, and may be an adjunct or alternative for patients whose spasticity or pain is not optimally managed," said Igor Grant, MD, director of the CMCR, which provided funding for the study.

Additional contributors include Tanya Wolfson, Anthony Gamst, PhD, Shelia Jin, MD, MPH, Thomas D. Marcotte, PhD, Heather Bentley and Ben Gouaux, all from UC San Diego School of Medicine.

— In the Journal of Clinical Investigation, an international team of scientists led by Dr Evan Reid at the University of Cambridge and Dr Stephan Zuchner from the University of Miami reports that mutations in the gene known as reticulon 2 on chromosome 19 cause a form of hereditary spastic paraplegia (HSP). HSP is characterised by progressive stiffness and contraction (spasticity) of the legs, caused by selective and specific degeneration of axons.

The team identified three mutations in the reticulon 2 gene as causing a type of HSP — in one case, this mutation included an entire deletion of the gene. In addition, the researchers showed that reticulon 2 interacts with another gene, spastin. Mutations in this gene cause the most common form of hereditary spastic paraplegia.

Reticulon 2 provides the genetic code for a reticulon protein that is a member of a family of proteins recently shown to have a key role in shaping the endoplasmic reticulum. The endoplasmic reticulum is a network of interconnected sheets and tubules that extends throughout the cytoplasm in nearly all cells.

The endoplasmic reticulum has several functions, including protein synthesis, calcium signalling and the regulation of other components of the cell. Recent data suggest the sheets are involved in protein synthesis, whereas the tubules are specialised to carry out the other functions.

This new study provides the most direct evidence to date that defects in how the endoplasmic reticulum is shaped and formed could underlie axon degeneration. When axons degenerate, signals are unable to pass through the nerve cells, leading to a breakdown of communication within the central nervous system. This is common in degenerative diseases of the nervous system, such as multiple sclerosis.

"Our work highlights important new disease mechanisms, which may provide a platform for us to study how axons are damaged in devastating illnesses such as HSP, and perhaps even in multiple sclerosis, which in some cases is very similar to HSP," explains Dr Reid, a Wellcome Trust Senior Research Fellow in Clinical Science. "But we must not forget how this work may immediately directly benefit families affected by HSP, for whom the discovery now opens up the possibility of genetic counselling and testing."

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Journal Reference:

1. Montenegro G et al. Mutations in the ER-shaping protein reticulon 2 cause the axon-degenerative disorder hereditary spastic paraplegia type 12. J Clin Invest, 2012

 Low vitamin D levels are associated with an increased risk of developing multiple sclerosis (MS), but the first randomized, controlled trial using high-dose vitamin D in MS did not find any added benefit over and above ongoing low-dose vitamin D supplementation, according to a study published in the Oct. 25, 2011, issue of Neurology®, the medical journal of the American Academy of Neurology.

"We did not find added benefit from high-dose vitamin D over and above ongoing low-dose vitamin D supplementation, but these results need to be confirmed with larger studies," said Mark S. Stein, MBBS, PhD, FRACP, of The Royal Melbourne Hospital and The Walter and Eliza Hall Institute of Medical Research in Parkville, Australia.

The six-month study involved 23 people with the relapsing-remitting form of MS. All of the participants received low-dose vitamin D (1,000 international units daily) to prevent any vitamin D deficiency. Half of the participants also received high-dose vitamin D2 to elevate their blood vitamin D to high levels (with a target serum 25-hydroxyvitamin D level of 130-175nM). The other half received a placebo high-dose.

MRI scans of the participants' brains were performed at the start of the study and again after four, five and six months. There was no significant difference between the two groups in the number of new abnormalities that had formed in the brain after six months and no significant difference in the change in the total volume of brain abnormalities.

Four of the 11 people taking the high-dose vitamin D, or 37 percent, had a relapse where their MS symptoms worsened during the study, while none of the 12 people taking only low-dose vitamin D had any relapses.

Stein noted that the study involved people who had MS for an average of six years. "It's possible that studies of high-dose vitamin D at an earlier stage of MS may lead to different results," he said.

This study was supported by The Myer Foundation in Melbourne, Australia.

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Journal Reference:

1. M. S. Stein, Y. Liu, O. M. Gray, J. E. Baker, S. C. Kolbe, M. R. Ditchfield, G. F. Egan, P. J. Mitchell, L. C. Harrison, H. Butzkueven, T. J. Kilpatrick. A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis. Neurology, 2011; 77 (17): 1611-1618 DOI: 10.1212/WNL.0b013e3182343274

Osteoporosis and low bone density are common in people in the early stages of multiple sclerosis (MS), according to a new study published in the July 12, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

"We've known that people who have had MS for a long time are at a greater risk of low bone density and broken bones, but we didn't know whether this was happening soon after the onset of MS and if it was caused by factors such as their lack of exercise due to lack of mobility, or their medications or reduced vitamin D from lack of sun exposure," said study author Stine Marit Moen, MD, of Oslo University Hospital Ulleval in Norway.

Low vitamin D levels are associated with an increased risk of MS. Low vitamin D levels can lead to reduced calcium absorption and bone mineralization, or the process the body uses to turn minerals into bone structure.

"Our hypothesis was that if vitamin D exerts a major effect on the risk of MS, then the effects of low vitamin D levels on bone density would be apparent soon after the onset of MS," Moen said.

The study involved 99 people with an average age of 37 who were recently diagnosed with MS or clinically isolated syndrome, which means they had a first episode of symptoms like those in MS but have not yet been diagnosed with the disease. All had no or minor physical disability from the disease.

The participants had bone density tests an average of 1.6 years after the first time they had any symptoms suggestive of MS. Their tests were compared to bone tests of 159 people of similar age, gender and ethnicity who did not have the disease.

A total of 51 percent of those with MS had either osteoporosis or osteopenia, compared to 37 percent of those who did not have the disease. Osteoporosis is a disease where low bone density causes the bones to become thin and brittle, making them more likely to break. Osteopenia is low bone density that is less severe than osteoporosis but puts a person at risk for osteoporosis.

The results remained the same after researchers adjusted for other factors that can affect bone density, such as smoking, alcohol use and hormone treatment.

"These results suggest that people in the early stages of MS and their doctors need to consider steps to prevent osteoporosis and maintain good bone health," Moen said. "This could include changing their diet to ensure adequate vitamin D and calcium levels, starting or increasing weight-bearing activities and taking medications."

The study was supported by the South-Eastern Norway Regional Health Authority, Ulleval University Hospital, Odd Fellow Research Foundation for Multiple Sclerosis, Endowment of K. and K. H. Hemsen and Endowment of Fritz and Ingrid Nelson.

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Journal Reference:

1. S. M. Moen, E. G. Celius, L. Sandvik, L. Nordsletten, E. F. Eriksen, T. Holmoy. Low bone mass in newly diagnosed multiple sclerosis and clinically isolated syndrome. Neurology, 2011; 77 (2): 151 DOI: 10.1212/WNL.0b013e3182242d34

Scientists at The University of Nottingham have discovered a molecular mechanism which could bring about the development of new treatments for multiple sclerosis (MS) — a chronic inflammatory disease of the central nervous system.

Dr Bruno Gran, a Clinical Associate Professor in the Division of Clinical Neurology in the School of Clinical Sciences, working in collaboration with Professor Paul Moynagh from the National University of Ireland, Maynooth, has discovered a synthetic chemical compound which inhibits the pro-inflammatory signals produced by the immune system in MS. What makes this chemical unique is that at the same time, it stimulates the body to produce interferon-beta, an anti-inflammatory molecule, that is commonly given to patients as an injected drug to treat MS.

Together, these effects cause significant reduction in the severity of an animal model of MS. The researchers have also discovered that cells of the immune system obtained from the blood of people with MS are more sensitive to the effects of this drug than those obtained from people who do not have MS.

Dr Gran said: "Under laboratory conditions we have found a way of encouraging the body to produce its own Interferon-beta. When other experimental substances have been tested in the laboratory to achieve this effect, they usually cause the immune system to produce a mixture of anti-inflammatory as well as pro-inflammatory molecules, typically reducing the overall efficacy. In the case of the compound tested in this study (a synthetic cannabinoid known as R(+)WIN55,212-2), the predominantly anti-inflammatory effects appear promising for further pre-clinical, and hopefully clinical, testing.

With no available cure MS is the focus of intense study for the hundreds of scientists across the world who are working on new treatments for this disabling disease. MS is more common in temperate climates. With around 100,000 people suffering from MS in the UK the country has one of the highest rates of the disease in the world.

Until 20 years ago there was little progress in the search for treatments.

After their first approval in 1993 beta Interferons still represent one of the first line treatments for relapsing-remitting multiple sclerosis. These drugs are not a cure but they can reduce the number and severity of relapses. Despite this, more effective, well tolerated therapeutic strategies are needed.

Dr Gran's research, published in the Journal of Biological Chemistry, continues a line of investigation which his laboratory has carried out for a number of years on the role of endogenous type I interferons in regulating multiple sclerosis inflammation in the central nervous system.

The cause of MS is still something of a mystery. Numerous factors are thought to contribute, including genetic susceptibility and environmental factors. The latter are thought to include certain viral infections and low levels of vitamin D, linked to poor sun exposure.

These latest findings highlight a new selective mechanism that may be open to exploitation in the development of new therapeutics for the treatment of MS.

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Journal Reference:

1. E. J. Downer, E. Clifford, B. Gran, H. J. Nel, P. G. Fallon, P. N. Moynagh. Identification of the Synthetic Cannabinoid R( )WIN55,212-2 as a Novel Regulator of IFN Regulatory Factor 3 Activation and IFN-  Expression: RELEVANCE TO THERAPEUTIC EFFECTS IN MODELS OF MULTIPLE SCLEROSIS. Journal of Biological Chemistry, 2011; 286 (12): 10316 DOI: 10.1074/jbc.M110.188599

Environmental and inherited risk factors associated with multiple sclerosis — previously poorly understood and not known to be connected — converge to alter a critical cellular function linked to the chronic neurologic disease, researchers with the UC Irvine Multiple Sclerosis Research Center have discovered.

The findings, which appear in the online, open-access journal Nature Communications, suggest that a unifying mechanism may be responsible for multiple sclerosis and point to therapies personalized according to genetic factors.

"MS results from complex interactions between an individual's genetics and his or her environment," said study leader Dr. Michael Demetriou, a UCI neurologist and associate director of the Multiple Sclerosis Research Center. "Defining how these come together to induce the disease is critical for developing a cure. We've taken a giant first step toward understanding this."

Using blood samples from about 13,000 people, Demetriou and colleagues identified the way environmental factors — including metabolism and vitamin D3, obtained through either sunlight exposure or diet — interact with four genes (interleukin-7 receptor-alpha, interleukin-2 receptor-alpha, MGAT1 and CTLA-4) to affect how specific sugars are added to proteins regulating the disease.

Earlier work on mice by Demetriou revealed that changes in the addition of these specific sugars to proteins engender a spontaneous MS-like disease. They also found that N-acetylglucosamine (GlcNAc), a dietary supplement and simple sugar related to glucosamine, is able to suppress this process.

The current research shows that both vitamin D3 and GlcNAc can reverse the effects of four human MS genetic factors and restore the normal addition of sugars to proteins. "This suggests that oral vitamin D3 and GlcNAc may serve as the first therapy for MS that directly targets an underlying defect promoting disease," Demetriou said.

Virtually all proteins on the surface of cells, including immune and nervous system cells, are modified with complex sugars of variable lengths and composition. This adds information to proteins separate from that directly defined by the genome. The sugars interact with specific sugar-binding proteins on the cell, forming a molecular lattice that controls the clustering, signaling and surface expression of critical receptors and transporters, such as the T cell receptor and CTLA-4. Reducing sugar modification weakens the lattice and enhances growth and activity of immune system T cells in such a way that they increase neural degeneration — a hallmark of MS.

Production of the complex sugars is regulated by both metabolic and enzymatic functions, the latter altered by genetic MS risk factors and vitamin D3. Demetriou pointed out that the MGAT1 genetic variant linked to MS increases or decreases the sugars attached to proteins depending on metabolism — one possible explanation for why people with the same genetic risk factor may or may not develop MS.

These sugars have also been implicated in many other chronic diseases, such as diabetes and cancer, Demetriou added, so this work could open up entirely new areas of medicine.

Haik Mkhikian, Ani Grigorian, Carey F. Li, Hung-Lin Chen, Barbara Newton, Raymond W. Zhou, Sevan Torossian, Gevork Grikor Tatarian, Sung-Uk Lee, Christine Beeton, K. George Chandy and Zhaoxia Yu of UCI and Ken Lau, Erin Walker, Katherine A. Siminovitch and James W. Dennis of the Samuel Lunenfeld Research Institute in Toronto participated in the study, which received support from the National Institute of Allergy & Infectious Diseases and the National Multiple Sclerosis Society, among others.

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Journal Reference:

1. Haik Mkhikian, Ani Grigorian, Carey F. Li, Hung-Lin Chen, Barbara Newton, Raymond W. Zhou, Christine Beeton, Sevan Torossian, Gevork Grikor Tatarian, Sung-Uk Lee, Ken Lau, Erin Walker, Katherine A. Siminovitch, K. George Chandy, Zhaoxia Yu, James W. Dennis, Michael Demetriou. Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis. Nature Communications, 2011; 2: 334 DOI: 10.1038/ncomms1333

— African-Americans who have multiple sclerosis (MS) have lower vitamin D levels than African-Americans who don't have the disease, according to a study published in the May 24, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology. However, most of the difference in vitamin D levels was due to differences in climate and geography.

"MS is not as common in African-Americans as it is in whites, although the disease tends to be more severe in African-Americans," said study author Ari J. Green, MD, of the University of California San Francisco and a member of the American Academy of Neurology. "We have known that vitamin D levels are associated with MS and that African-Americans are at increased risk for having low vitamin D levels, but little research has been done to look at vitamin D levels in African-Americans with MS."

Melanin, which determines the level of pigment in the skin, acts as a filter of UV light, which limits the amount of vitamin D that can be produced by the body in response to sunlight.

The study involved 339 people with MS and 342 people who did not have the disease. Researchers looked at vitamin D levels in the blood, the severity of the disease, the amount of UV exposure for participants based on where they lived and the proportion of European genetic ancestry participants had.

A total of 77 percent of the people with MS were vitamin D deficient, compared to 71 percent of those without the disease. The people with MS were exposed to a lower monthly UV index (average of 3.8) than those without the disease (average of 4.8). They also lived an average of about one degree of latitude farther north than those without the disease. The link between low vitamin D levels and MS was weaker, but still present after adjusting for the differences in UV exposure and geography.

People with a higher proportion of European ancestry in their genes were less likely to have low vitamin D levels than people with a lower proportion of European ancestry, but European ancestry was not associated with MS.

There was no association between vitamin D levels and how severe the disease was.

People should talk to their physicians about blood testing for vitamin D levels, whether they should take supplements and how much UV exposure they should get, Green said. "These findings may provide a mechanism to help explain how genes and the environment interact to produce MS," he said.

The study was supported by the American Academy of Neurology Foundation/National Multiple Sclerosis Society Clinician-Scientist Development Award, the National Institutes of Health, the National Multiple Sclerosis Society and a University of California San Francisco Resident Research grant.

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Journal Reference:

1. J. M. Gelfand, B. A. C. Cree, J. McElroy, J. Oksenberg, R. Green, E. M. Mowry, J. W. Miller, S. L. Hauser, A. J. Green. Vitamin D in African Americans with multiple sclerosis. Neurology, 2011; 76 (21): 1824 DOI: 10.1212/WNL.0b013e31821cccf5

— Researchers at the University of California, San Diego School of Medicine have discovered a steroid hormone that inhibits inflammation in the brain. The findings, to be published in the May 13 issue of the journal Cell, have implications for understanding the exaggerated inflammatory responses that are characteristic features of numerous neurodegenerative diseases.

The discovery that the steroid hormone ADIOL, (5-androsten-3Β-17Β-diol), a precursor of androgens and estrogens, modulates inflammation induced by microglia cells could eventually lead to new treatments for patients with neurodegenerative conditions in which inflammation plays a pathogenic role. In addition, levels of ADIOL in blood or other body fluids might be useful for predicting risk or responses to drugs that mimic its actions.

The senior author of the paper is Christopher Glass, MD, PhD, professor of the department of cellular and molecular medicine and the department of medicine. Lead author is Kaoru Saijo, MD, PhD, and an associate project scientist in the Glass lab.

Though neurons get the headlines, they thrive only with the support of other cell types, among them microglia and astrocyte cells. Microglial cells help the central nervous system respond to infection and injury. Under normal conditions, they exist in a resting state, quietly but constantly surveying their surrounding environment for tell-tale indications of microbial invasion or tissue damage. Once detected, microglia initiate an inflammatory response, kick-starting immune system and tissue repair processes. Astrocytes amplify the immune reaction launched by microglia.

The microglia-astrocyte activation is vital to an effective immune response and damage repair, but if the resulting inflammation induced by these cells is not controlled or goes on too long, it can result in damage and death to neurons. Inflammation run amok is linked to many neurodegenerative diseases, such as Parkinson's disease, HIV-associated dementia, Alzheimer's disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and some inflammatory diseases like multiple sclerosis (MS).

The new findings suggest that in healthy brains, microglia inflammation is modulated by the production of the steroid hormone ADIOL, which instructs support cells to calm down and return to their quiescent state. ADIOL works by binding to a transcription factor called estrogen receptor Β, which gets its name because of its similarity to estrogen receptor Β and its ability to bind to the female sex hormone estrogen. Unexpectedly, while ADIOL binding causes estrogen receptor α to execute an anti-inflammatory set of instructions to microglia and astrocytes, estrogen binding does not. Because of this, estrogens can actually antagonize the anti-inflammatory actions of ADIOL.

Glass and Saijo made their discovery based upon initial studies with John Katzenellenbogen, PhD, at the University of Illinois, Urbana-Champaign. Kaztenellenbogen's laboratory developed a number of synthetic small molecules that could bind very tightly and specifically to estrogen receptor .

Saijo at UC San Diego tested each of these compounds and found that some were potent inhibitors of inflammatory responses of microglia and astrocytes, while others were not. When one of these compounds was tested in vivo, it was found to strongly inhibit inflammation in the brain and to induce remission in a mouse model of multiple sclerosis.

Although estrogen itself can be neuroprotective, its lack of ability to induce the anti-inflammatory activity of estrogen receptor  led to a search for endogenous or internal molecules that might have similar activities to the synthetic compounds. Saijo worked with Andrew Li, MD, assistant adjunct professor of medicine at UC San Diego, to ultimately identify ADIOL as the endogenous regulator of estrogen receptor  activity. Notably, Saijo and Li found that the amount of ADIOL that could be produced by microglia was regulated by signals that control the magnitude and duration of inflammatory responses

"We think it possible that mutations in the genes encoding the key enzymes for the generation of ADIOL, or their inappropriate down-regulation, could contribute to pathological forms of inflammation," Glass said.

These findings raise the possibility that women are more susceptible to certain inflammatory diseases, such as MS, because their higher levels of estrogens potentially antagonize the anti-inflammatory actions of ADIOL in the brain. A similar argument might also help explain some of the adverse effects of estrogen administration on the brain in post-menopausal women.

Glass noted, however, that much research remains to be done. The precise relationship between brain inflammation and neurodegenerative disease, for example, is not fully understood. Similarly, it's not known whether people naturally produce different amounts of ADIOL. And researchers have only identified the ADIOL-estrogen connection in an MS mouse model. Glass said he and colleagues will next look at animal models for Alzheimer's, Parkinson's and HIV-dementia.

Co-authors of the study include Jana G. Collier, UCSD Department of Cellular and Molecular Medicine.

Funding for this study was provided by the National Institutes of Health.

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Journal Reference:

1. Kaoru Saijo, Jana G. Collier, Andrew C. Li, John A. Katzenellenbogen, Christopher K. Glass. An ADIOL-ERβ-CtBP Transrepression Pathway Negatively Regulates Microglia-Mediated Inflammation. Cell, 2011; 145 (4): 584-595 DOI: 10.1016/j.cell.2011.03.050

— Researchers including members from the Niels Bohr Institute at the University of Copenhagen have developed a new method for making detailed X-ray images of brain cells. The method, called SAXS-CT, can map the myelin sheaths of nerve cells, which are important for conditions such as multiple sclerosis and Alzheimer's disease. The results have been published in the scientific journal, NeuroImage.

The myelin sheaths of nerve cells are lamellar membranes surrounding the neuronal axons. The myelin layers are important to the central nervous system as they ensure the rapid and uninterrupted communication of signals along the neuronal axons. Changes in the myelin layers are associated with a number of neurodegenerative disorders such as cerebral malaria, multiple sclerosis, and Alzheimer's disease.

The development of these diseases are still not fully understood, but are thought to be related to the damage of the myelin layers, so that messages from the brain reach the various parts of the body poorly or not at all. It is like an electric cord where the insulating material has been damaged and the current short circuits. In order to find methods to prevent or treat the diseases it is important to understand the connection between the diseases and the changes in the myelin.

Getting 3-D X-ray images

"We have combined two well-known medical examination methods: SAXS (Small-Angle X-ray Scattering) and CT-scanning (computed tomography scanning). Combined with a specially developed programme for data processing, we have been able to examine the variations of the myelin sheaths in a rat brain all the way down to the molecular level without surgery," explains PhD Torben Haugaard Jensen, Niels Bohr Institute at the University of Copenhagen. The method is called 'Molecular X-ray CT', because you use X-ray CT to study myelin at the molecular level.

The research has been carried out in collaboration with researchers in Switzerland, France and Germany. The experiments took place at the Paul Scherrer Institute in Switzerland, where they have a powerful X-ray source that can measure Small-Angle X-Ray Scattering, SAXS at a high resolution. Normally such experiments would give two-dimensional X-ray images that are sharp and precise, but without information on depth. But by incorporating the method from CT-scanning, where you image from different angles, the researchers have managed to get 3D X-ray images.

This has not only required the development of new X-ray methods and experiments, but has also required the development of new methods for processing data. The extremely detailed measurements of cross sections from different angles meant that there were 800,000 images to be analysed. So the researchers have also developed an image-processing programme for the SAXS-CT method. The result is that they can see all of the detailed information from SAXS in spatially resolved.

From point samples to total samples

"We can see the myelin sheaths of the neuronal axons and we can distinguish the layers which have a thickness of 17.6 nanometers," explains Torben Haugaard Jensen. "Up until now, you had to cut out a little sample in order to examine the layers in one area and get a single measuring point. With the new method we can examine 250,000 points at once without cutting into the sample. We can get a complete overview over the concentration and thickness of the myelin and this gives of the ability to determine whether the destruction of the myelin is occurring in spots or across the entire sample," he explains.

The research provides new opportunities for collaboration with doctors at Copenhagen University Hospital and the Panum Institute, who they already have close contact with. The method cannot be used to diagnose living persons. But the doctors can obtain new knowledge about the diseases, what kind of damage is taking place? — and where? They will be able to follow the development of the diseases and find out how the brain is being attacked. This knowledge could perhaps be used to develop a treatment.

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Journal Reference:

1. T.H. Jensen, M. Bech, O. Bunk, A. Menzel, A. Bouchet, G. Le Duc, R. Feidenhans'l, F. Pfeiffer. Molecular X-ray computed tomography of myelin in a rat brain. NeuroImage, 2011; DOI: 10.1016/j.neuroimage.2011.04.013

New research suggests that people who are exposed to low levels of sunlight coupled with a history of having a common virus known as mononucleosis may be at greater odds of developing multiple sclerosis (MS) than those without the virus. The research is published in the April 19, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

"MS is more common at higher latitudes, farther away from the equator," said George C. Ebers, MD, with the University of Oxford in the United Kingdom and a member of the American Academy of Neurology. "Since the disease has been linked to environmental factors such as low levels of sun exposure and a history of infectious mononucleosis, we wanted to see whether the two together would help explain the variance in the disease across the United Kingdom."

Infectious mononucleosis is a disease caused by the Epstein-Barr virus, which is a Herpes virus that is extremely common but causes no symptoms in most people. However, when a person contracts the virus as a teenager or adult, it often leads to infectious mononucleosis. The body makes vitamin D when exposed to ultraviolet B (UVB) light.

For the study, researchers looked at all hospital admissions to National Health Service hospitals in England over seven years. Specifically, they identified 56,681 cases of multiple sclerosis and 14,621 cases of infectious mononucleosis. Scientists also looked at NASA data on ultraviolet intensity in England.

The study found that adding the effects of sunlight exposure and mononucleosis together explained 72 percent of the variance in the occurrence of MS across the United Kingdom. Sunlight exposure alone accounted for 61 percent of the variance.

"It's possible that vitamin D deficiency may lead to an abnormal response to the Epstein-Barr virus," Ebers said.

He noted that low sunlight exposure in the spring was most strongly associated with MS risk. "Lower levels of UVB in the spring season correspond with peak risk of MS by birth month. More research should be done on whether increasing UVB exposure or using vitamin D supplements and possible treatments or vaccines for the Epstein-Barr virus could lead to fewer cases of MS."

The study was supported by the Multiple Sclerosis Society of Great Britain and Northern Ireland, the Medical Research Council and the Wellcome Trust.

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Journal Reference:

1. Ramagopalan, S.V., Handel, A.E., Giovannoni, G., Siegel, S., Ebers, G.C., MD, FMedSci, Chaplin, G. Relationship of UV exposure to prevalence of multiple sclerosis in England. Neurology, April 19, 2011; Pages: 1410-1414