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    You are here : Home » MS Research News » New Discoveries » Cerebro-Spinal Fluid & Spinal Cord

    Cerebro-Spinal Fluid & Spinal Cord

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    Mayo clinic finds tool to predict disability timeline for progressive MS

    Lumbar PunctureMany patients with progressive multiple sclerosis (MS) worry how quickly the disease will progress. Now, by noting the presence of certain markers in a commonly performed diagnostic test, Mayo Clinic researchers can predict whether patients will suffer a faster onset of disability and counsel them to help ease anxiety. The research is being presented at the American Academy of Neurology meeting in Honolulu, Hawaii.

    Progressive MS is a disease of the central nervous system that can damage the brain, spinal cord and optic nerves. Over time, this damage can make it difficult or impossible for patients to walk, making them reliant on mobility aids such as walkers or wheelchairs.

    "In this study, we found that in patients who developed the progressive form of MS that had preceding relapses, the presence of greater production of one of these molecules, immunoglobulin G, predicted a faster onset of disability," explains Orhun Kantarci, M.D., a Mayo Clinic neurologist and the study's lead author. As physicians better predict the onset of disability, they can better counsel patients by providing answers in a time of uncertainty.

    The study looked at cerebrospinal fluid (CSF) test results from a sample of 281 progressive MS patients seen at Mayo Clinic from 2002 to 2007. In general, CSF test results help physicians when the diagnosis is uncertain. For this study, researchers analyzed CSF test results and noticed a relationship between a faster disability rate and abnormally high levels of two proteins -- oligoclonal band and immunoglobulin-G molecule. If patients had the progressive form of MS with proceeding relapses, and their CSF results showed an elevated protein, researchers concluded they will have a faster rate of disability.

    The study is a significant step forward in predicting disability outcomes, says researcher Junger Tang, M.D., a neurology fellow at Mayo Clinic. The next step is further research to confirm the results, he says.

    MS is the most common cause of nontraumatic neurological disability in young adults in North America and Europe. MS occurs most often in people ages 20 to 40, and is up to three times more common in women than men. Symptoms include weakness, loss of sensation, visual disturbances, and cognitive dysfunction.

    Source: Medical News Today © MediLexicon International Ltd 2004-2011 (13/04/11)

    Differential expression of complement proteins in CSF from active MS patients

    <umbar PunctureAbstract
    Multiple sclerosis (MS) is a demyelinating disease of the central nervous system with complex immunopathogenesis. Using the 2-D DIGE technology, we separate CSF proteins from patients with active MS and control subjects.

    Three of the seven differential proteins identified were related with complement system, and the network analysis of the differential proteins revealed complement activation involvement in active MS.

    Complement C4b (gamma chain) was confirmed elevated by performing western blotting analysis (p<0.01). The present results are an independent quantitative proteomic measure in CSF from active MS patients. The differential expression of the complement C4b and related proteins in CSF provides potential biomarkers as well as evidence for the involvement of complement activation in the pathogenesis of MS disease.

    Multiple sclerosis (MS) is a common demyelinating disease of the central nervous system (CNS) with complex immunopathogenesis, in which the myelin sheaths and axons are destroyed with unclear aetiology and pathogenesis [Tumani et al., 2009].

    The disorder results from an interplay between as yet unidentified environmental factors and susceptibility genes.

    Up to now, MS is recognized throughout the world, with around 2.5 million affected individuals. It is a potentially disabling disease for young adults [Compston and Coles, 2002]. Relapsing-remitting MS (RRMS) is the most common clinical subtype which is characterized by a series of exacerbations that result in varying degrees of disability [Ottervald et al., 2010]. Previous studies revealed that poor recovery from the first two attacks of MS is the most important significant single risk factor for disease progression [Mowry et al., 2009; Scott and Schramke, 2010], and it is hoped that treating patients during the early phase of MS may provide an opportunity to prevent relapses [Vollmer, 2007]. Therefore, earlier diagnosis and new therapeutic strategies are urgently needed for MS, especially in the crucial early stages of the illness.

    Complement plays a central role in the innate immune system, providing an important defense against infection and immune complex disease including MS [Gasque et al., 2000]. Within the CNS the majority of complement proteins are produced by glial cells and neurones and expression is increased in response to inflammation [Morgan et al. 1996; Gasque et al. 2000]. In patients with MS, numerous studies have indicated that there is a change in complement activity in CSF or serum. However, the actual pathogenic role of complement in MS remains poorly understood.

    Results obtained from different studies measuring the same complement component (C3 and C4) have often been conflicting, which were reviewed in detail by Ingram [Ingram et al., 2009]. In two latest studies, a fragment of C4 was found increased in serums of MS [Sawai et al., 2010], and plasma and CSF levels of C4a were elevated in acute RRMS [Ingram et al., 2010]. This indicates the potential role of C4 related proteins as biomarker of MS.

    To find new biomarkers for MS and the possible pathogenesis, we studied CSF proteins of active MS patients and controls by two-dimensional fluorescence differential in gel electrophoresis (2-D DIGE). This approach is based on the separation of proteins pre-labeled with fluorescent dyes according to their charge in a first dimension by isoelectric focusing (IEF) and according to their size in a second dimension by SDS polyacrylamide gel electrophoresis (SDS-PAGE) [Marouga et al., 2005; Shaw et al., 2009]. In this unbiased approach, abnormal expression of seven proteins was found in CSF from patients with active MS and controls with other neurological disorders (ONDs).

    The protein-protein interactive network analysis of the seven differential proteins revealed complement activation involvement. Our results provide independent evidence for involvement of complement activation in active MS, and these findings may have a relevant impact on the identification of disease-specific biomarkers.

    Full article -

    Yun Li1, Zhaoyu Qin2, Mingchong Yang1, Yanjiang Qin3, Chengzhao Lin2, Shilian Liu1

    1Institute of Biochemistry and Molecular Biology, School of Medicine, Shandong University, China
    2Laboratory of Systems Biology, Institute of Biomedical Sciences, Fudan University, China
    3Department of Neurology, Qilu Hospital of Shandong University, China

    Source: Journal Of Cellular Biochemistry DOI: 10.1002/jcb.23113 © 2011 Wiley-Liss, Inc. (29/03/11)

    Spinal cord ring enhancement in multiple sclerosis

    Spinal Cord ImageRing enhancement is a recognised radiological feature of MS lesions. However it is more commonly associated with other pathologies and its presence often results in additional investigation for patients.

    The authors attempted to categorise the specific features of ring enhancing lesions in the spinal cord of patients with MS by conducting a retrospective analysis of 322 spinal cord scans performed over a three year period.

    Ring enhancement was seen in 20 patients with spinal cord enhancement, most commonly in the cervical cord. Incomplete or "open" ring enhancement was the dominant pattern in 19 of the 20 patients (95%). Concurrent enhancing brain lesions were present in 14 patients, 8 of which (57%) exhibited a ring pattern of enhancement.

    The authors concluded that as the most common pattern of enhancement seem was incomplete ring enhancement in the cervical spinal cord, recognition of this pattern may improve and expedite the diagnosis of MS and preclude the need for invasive diagnostic interventions.

    Authors: Klawiter EC, Benzinger T, Roy A, Naismith RT, Parks BJ, Cross AH.

    Source: Arch Neurol. 2010 Nov;67(11):1395-8. (17/11/10)

    Predictive factors for MS in patients with clinically isolated spinal cord syndrome

    Lumbar PunctureAbstract
    Objectives: To identify predictors of conversion to definite multiple sclerosis (MS) in patients with a cord clinically isolated syndrome.

    Methods: The predictive values for conversion to MS of clinical, magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) variables in 114 patients with acute partial myelitis confirmed by a spinal cord lesion on MRI were studied. Other causes of cord syndromes were excluded.

    Results: MS was diagnosed in 78 patients (86%) during 4.0 ± 1.9 years of follow-up. Some 67 of these patients had a second clinical episode. The diagnosis of isolated myelitis was maintained for 36 patients, 78% of whom (28 cases) were followed for at least 2 years, comparable to the MS patients. Age, bladder involvement, ≥2 cord lesions on MRI, ≥9 brain lesions, ≥3 periventricular lesions and intrathecal IgG synthesis predicted conversion to clinically definite MS. Multivariate logistic analysis identified three predictors of MS diagnosis: age ≤40 years, inflammatory CSF and ≥3 periventricular lesions on brain MRI.

    Conclusion: Two out of three baseline factors (age, periventricular lesions and inflammatory CSF) predicted conversion to MS with better accuracy than the revised McDonald criteria for dissemination in space.

    Ruet A, Deloire MS, Ouallet JC, Molinier S, Brochet B.

    Services de Neurologie et de Neuro-imagerie, Hôpital Pellegrin, CHU de Bordeaux, France.

    Source: Multiple Sclerosis 2010 Nov 11 & Pubmed PMID: 21071465 (17/11/10)

    Hypogelsolinemia, a disorder of the extracellular actin scavenger system, in patients with MS

    Lumbar PunctureExtracellular gelsolin (GSN) and GC-globulin /Vitamin D-binding protein (DBP) appear to play an important role in clearing the actin from extracellular fluids and in modulating cellular responses to anionic bioactive lipids.

    In this study we hypothesized that cellular actin release and/or increase in bioactive lipids associated with multiple sclerosis (MS) development will translate into alteration of the actin scavenger system protein concentrations in blood and cerebrospinal fluid (CSF) of patients with MS.

    Methods: We measured GSN and DBP concentrations in blood and CSF obtained from patients diagnosed with MS (n=56) in comparison to a control group (n=20) that includes patients diagnosed with conditions such as idiopathic cephalgia (n=11), idiopathic (Bell's) facial nerve palsy (n=7) and ischialgia due to discopathy (n=2).

    GSN and DBP levels were measured by Western blot and ELISA, respectively.

    Results: We found that the GSN concentration in the blood of the MS group (115+/-78 ug/ml) was significantly lower (p<0.001) compared to the control group (244+/-96 ug/ml). In contrast, there was no statistically significant difference between blood DBP concentrations in patients with MS (310+/-68 ug/ml) and the control group (314+/-82 ug/ml).

    GSN and DBP concentrations in CSF also did not significantly differ between those two groups.

    Conclusions: The decrease of GSN concentration in blood and CSF of MS subjects suggests that this protein may be involved in chronic inflammation associated with neurodegeneration. Additionally, the results presented here suggest the possible utility of GSN evaluation for diagnostic purposes.

    Reversing plasma GSN deficiency might represent a new strategy in MS treatment.

    Author: Alina KulakowskaNicholas CiccarelliQi WenBarbara MroczkoWieslaw DrozdowskiMaciej SzmitkowskiPaul JanmeyRobert Bucki
    Credits/Source: BMC Neurology 2010, 10:107

    Source: 2010 7thSpace Interactive © 2010 7thSpace Interactive (02/11/10)

    Abnormalities in the cerebrospinal fluid levels of endocannabinoids in Multiple Sclerosis
    OBJECTIVE: Endocannabinoids (eCBs) play a pivotal role in the modulation of neuroinflammation and experimental findings suggest that they may be directly involved in the pathogenesis of multiple sclerosis (MS). The objective of our study was to measure eCBs levels in the cerebrospinal fluid (CSF) of MS patients.

    PATIENTS AND METHODS: Arachidonoyl-ethanolamide (anandamide, AEA), palmitylethanolamide (PEA), 2-arachidonoyl-glycerol (2-AG) and oleoylethanolamide (OEA) levels were measured in the CSF of 50 MS patients and 20 control subjects by isotope dilution gas-chromatography/mass-spectrometry. Patients included thirty-five MS patients in the relapsing-remitting (RR) form of the disease, 20 in a stable clinical phase and 15 during a relapse, and 15 MS patients in the secondary progressive form (SP).

    RESULTS: Significantly reduced levels of all the tested eCBs were found in the CSF of MS patients compared to control subjects, with lower values detected in the SP MS group. Higher levels of AEA and PEA, although below those of controls, were found in the CSF of RR MS patients during a relapse. Higher levels of AEA 2-AG and OEA were found in patients with MRI gadolinium-enhancing (Gd+) lesions.

    DISCUSSION: The present findings suggest the presence of an impaired eCB system in MS. Increased CSF levels of AEA during relapses or in RR patients with Gd+ lesions suggest its potential role in limiting the ongoing inflammatory process with potential neuroprotective implications. These findings provide further support for the development of drugs targeting eCBs as potential pharmacological strategy to reduce the symptoms and slow disease progression in MS.

    Di Filippo M, Pini LA, Pelliccioli GP, Calabresi P, Sarchielli P.
    Clinica Neurologica, Universita' di Perugia, Perugia, and IRCCS Fondazione S Lucia, Rome, Italy.

    Source: Pubmed PMID: 18535023 (18/06/08)

    Cerebrospinal fluid brain specific proteins in relation to nitric oxide metabolites during relapse of multiple sclerosis.
    This study investigated the cerebrospinal fluid (CSF) levels of ferritin, S100B as biomarkers for glial activation and NfH(SM135) - a biomarker of axonal damage - in relation to nitric oxide (NO) metabolites: nitrate and nitrite (NOx) during acute multiple sclerosis (MS) relapse.

    Thirty-four relapsing-remitting MS (RR-MS) patients during acute relapse and 12 controls were enrolled. Patients were assessed on Expanded Disability Status Scale (EDSS) and underwent lumbar puncture within two weeks following relapse.

    Twenty patients were available for further follow-up and were assessed on EDSS 6-8 weeks since the relapse onset. The CSF NOx (P < 0.0001), NfH(SM135) ( P = 0.01) and S100B (P = 0.009) but not ferritin (P > 0.05) were significantly raised in MS group.

    There was a significant correlation between CSF ferritin and S100B in RR-MS group (P = 0.004). CSF NOx did not correlate with S100B and ferritin in study groups. RR-MS patients with detectable NfH(SM135) levels had higher NOx compared with subjects having undetectable NfH(SM135) (P = 0.03). In the follow-up study, raised baseline levels of NOx (P = 0.016) or NfH(SM135) (P = 0.04) inversely correlated with the clinical recovery grade expressed as relative EDSS change between baseline and follow-up.

    In conclusion, NO metabolites were increased and because of their correlation with a biomarker of axonal degeneration (neurofilaments) and a measure for clinical disability (EDSS), relapse-related nitrosative stress is likely to be relevant to the development of sustained disability in an individual patient.

    Rejdak K, Petzold A, Stelmasiak Z, Giovannoni G.
    Department of Neurology, Medical University of Lublin, Lublin, Poland.

    Source: Multiple Sclerosis 2008; 14: 59-66. (09/01/08)

    Carbon monoxide protects mice from multiple sclerosis
    TITLE: Heme oxygenase–1 and carbon monoxide suppress autoimmune neuroinflammation

    Multiple sclerosis (MS) is a chronic inflammatory disorder that causes degeneration of the nerves in the brain and spinal cord, leading to various symptoms including muscle weakness and pain. Most individuals with MS go through cycles of disease and remission, leading to the suggestion that there are regulatory mechanisms that counter the disease-causing inflammation. Using a mouse model of MS (known as EAE), researchers from the Gulbenkian Institute in Portugal show that increased expression of a protein known as HO-1, as well as administration of carbon monoxide, protect mice from disease.

    In the study, which appears online on January 25 in advance of publication in the February print issue of the Journal of Clinical Investigation, Miguel Soares and colleagues show that mice lacking HO-1 develop more severe EAE than wild-type mice. Conversely, in mice already suffering the symptoms of EAE, disease is reversed if HO-1 expression is induced. The function of HO-1 is to degrade excess heme (a component of many important cellular proteins) and one of the by-products of heme degradation is carbon monoxoide. Surprisingly, like the induction of HO-1 expression, administration of carbon monoxide to mice already suffering the symptoms of EAE decreased disease. The authors therefore suggest that modulating HO-1 expression or administering carbon monoxide might be useful therapeutic strategies to treat patients with MS.

    Source: Journal of Clinical Investigation (26/01/07)

    Researchers Closer to Cure for Multiple Sclerosis and Other Myelin-related Diseases
    A breakthrough finding on the mechanism of myelin formation by Jonah Chan, assistant professor of cell and neurobiology at the Keck School of Medicine of the University of Southern California, could have a major impact on the treatment of diseases such as multiple sclerosis and demyelination as a result of spinal cord injuries.

    Myelin, the white matter that coats all nerves, allows long-distance communication in the nervous system. "It plays a vital role in the overall health and function of the nervous system, and its degeneration plays a role in a number of diseases, such as multiple sclerosis, peripheral neuropathies, and even in spinal cord injury," Chan explained.

    The study, "The Polarity Protein Par-3 Directly Interacts with p75NTR to Regulate Myelination", appears in the Nov. 3 issue of Science. Chan, who works at the Zilkha Neurogenetic Institute at the Keck School of Medicine of USC, collaborated on the study with Michel Cayouette and researchers at the Institut de Recherches Cliniques de Montreal in Canada.

    At a basic level, the nervous system functions like a collection of wires that transmit electrical signals encoding our thoughts, feelings, and actions. Just as an electrical wire needs insulation, myelin is wrapped around axons - the wire-like extensions of neurons that make up nerve fibres. The sheath helps to propagate the electrical signal and maximise the efficiency and velocity of these signals in our brain and body.

    Diseases and injuries that compromise the integrity of myelin, such as multiple sclerosis or peripheral neuropathies, have dramatic consequences like paralysis, uncoordinated movements, and neuropathic pain.

    Chan's study sheds light on the mechanisms that control how myelin is formed during development of the nerves. The article constitutes an important step forward in understanding the process of myelination and opens the way to new research in this field.

    Chan showed that a protein, Par-3, is at the base of the myelination process. This protein becomes localised to one side of the myelin-forming cells, known as Schwann cells, upon contact with the axon that is to be myelinated. Par-3 acts almost as a molecular scaffold to set-up an "organising centre", which brings together key proteins essential for myelination, in particular a receptor for a molecule secreted by the neurons.

    The researchers found that when they disrupted this organising centre, cells could not form myelin normally. Importantly, their discovery demonstrates that Schwann cells need to become polarised so that they know which side is in contact with the axon to initiate wrapping and to bring essential molecules to this critical interface.

    These studies open the way to new research, said Chan, which should help to identify other components that are recruited at the organising centre set-up by Par-3. In multiple sclerosis, or after injury, Schwann cells can re-myelinate axons of the central nervous system to some degree. Therefore, these experiments bring about the possibility that manipulating the Par-3 pathway might allow for more efficient re-myelination of damaged or diseased nerves.

    This work was supported by the National Multiple Sclerosis Society Career Transition Award and the Donald E. and Delia B. Baxter Foundation Award to Jonah Chan, and the Canadian Institute of Health Research to Michel Cayouette.

    Chan, J. R., Jolicoeur, C., Yamauchi, J, Elliott, J, Fawcett, J. P., Ng, B. K., and Cayouette, M. ,"The Polarity Protein Par-3 Directly Interacts with p75NTR to Regulate Myelination," Science, Nov. 3, 2006.

    Source: Newswise © 2006 Newswise. All Rights Reserved.(03/11/06)

    Hopes for protein in MS battle
    Experts believe they have discovered a protein which could help create new treatments for multiple sclerosis.

    It works by helping to form a fatty white coating called myelin, which is destroyed by the immune system in people with MS.

    The body's nerve fibres are sheathed in myelin - which both insulates and helps the passage of electrical signals.

    Now US experts have found a protein called Par-3 that underpins the formation of myelin.

    Dr Jona Chan, of the University of Southern California in Los Angeles, said: "Myelin plays a vital role in the overall health and function of the nervous system.

    "Its degeneration is a factor in a number of diseases such as multiple sclerosis, peripheral neuropathies and even in spinal cord injury."

    Par-3 acts as an "organising centre", bringing together key proteins essential for forming myelin.

    Scotland has one of the highest rates of MS in the world, with more than 10,000 people with the illness.

    Experts say cold weather, environment and genes are probably to blame for the increased incidence.

    Source: The Daily Record (03/11/06)

    12.5 kDa Cystatin May Generate First Simple Test for Multiple Sclerosis
    Johns Hopkins scientists report the discovery of a protein found only in cerebrospinal fluid that they say might be useful in identifying a subgroup of patients with multiple sclerosis (MS) or identifying those at risk for the debilitating autoimmune disorder.

    MS strikes over 10,000 Americans each year, most of whom are women, and causes weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and  bladder control. It is a disorder in which the immune system destroys myelin, the covering of nerves that helps transmit signals. Cerebrospinal fluid (CSF) is the watery fluid that surrounds and cushions the brain and spinal cord.

    The federally funded Hopkins research, reported in the February issue of the Annals of Neurology, is important, the researchers say, because unlike other autoimmune diseases in which the body attacks its own tissues, MS cannot be diagnosed with a simple blood or other test.

    While it is recognised that there might be several forms of MS, laboratory-based tests need to be developed to diagnose these subtypes.

    “There is the possibility now that the protein we identified, 12.5 kDa cystatin, can be used to diagnose MS, perhaps in its earliest stages, and also to monitor treatment by measuring its levels in CSF,” says Avindra Nath, M.D., a professor in the Department of Neurology at The Johns Hopkins University School of Medicine and lead author of the study.

    Working with human CSF, the Hopkins team showed that 12.5 kDa cystatin is a breakdown product of a larger protein called cystatin C or 13.4kDa, which in turn blocks activity of some enzymes, including cathepsin B. Cathepsin B has been linked to demyelination-the destruction of the nerve sheath. The term kDa refers to Kilodalton, the weight of one molecule of a substance.

    “In fact, those patients who had more of the breakdown product of 12.5 kDa cystatin also seemed to have the highest cathepsin B inhibition,” Nath said.

    The investigators made their finding using a sophisticated technique called SELDI-time-of-flight mass spectroscopy that can find one specific protein in a complex mixture based on its weight. They used it to examine CSF samples from 29 patients with MS or pre-MS  symptoms such as numbness on one side; 27 patients with transverse myelitis, a painful inflammation of spinal cord nerves; 50 infected with the AIDS virus (which can cause nerve damage); and 27 with other neurological diseases. The Hopkins scientists analyzed CSF instead of blood samples because CSF better represents local events in the brain than does blood, according to Nath. And the high concentrations of many proteins in the blood can mask proteins that might be biomarkers for MS, he added.

    The team found that the 12.5kDa fragment of cystatin C occurred in CSF samples from two-thirds of patients with MS or the pre-MS conditions. Moreover, although total cystatin C levels in MS patients were not different from control patients without the disease, patients with MS had a larger proportion of the 12.5 kDa compared to 13.4 kDa cystatin C than did other patients. Thus, the presence of the 12.5 kDa fragment might identify a subgroup of MS patients.

    The other authors of this study include Daniel N. Irani and Douglas A. Kerr, departments of Neurology and Molecular Microbiology and Immunology; Caroline Anderson, Justin C. McArthur, Ned Sacktor, Melina Jones and Peter Calabresi, Department of Neurology; Rebekah Gundry and Robert Cotter, Department of Pharmacology and Molecular Sciences; Stacy Moore, Ciphergen Biosystems Inc., Freemont, Calif.; Carlos A. Pardo, Departments of Neurology and Pathology.

    This study was supported by the National Institutes of Health, National Institute of Neurological Disorders and Stroke, the National Institute on Drug Abuse, the National Institute of General Medical Sciences, and by a Collaborative Center Grant from the National Multiple Sclerosis Society.

    Source: Johns Hopkins Medical Institutions © 2006 Newswise. All Rights Reserved. (03/03/06)

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