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Results for “SCLEROSIS, MULTIPLE”

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PubMed2001

No linkage or association of the nitric oxide synthase genes to multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) of unknown etiology. Nitric oxide (NO) is a free radical that participates in a variety of biological processes. It is an important mediator in the immune response. Several studies indicate involvement of NO in the pathogenesis of MS. We studied five markers within the three NO synthase genes with regards to susceptibility and disease course in 156 affected sib-pairs and in 96 "benign" and 96 "severe" definite MS patients and 148 controls. We found no significant association or evidence for linkage in our data sets.

Case-Control Studies↗

PubMed2003

Mutations in the gene for toll-like receptor 4 and multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system with heterogeneous pathological features, disease courses and genetical backgrounds. In this study we determined whether genetic variants of toll-like receptor (TLR) 4, which confer substantial differences in the inflammation elicited by bacterial lipopolysaccharide, are related to the development of MS. We found no differences in the frequencies of the cosegregating TLR4 Asp299Gly and Thr399Ile polymorphisms between Austrian MS patients (11.6%) and age-matched controls (13.7%). Furthermore, we could not detect any influence of these mutations on clinical parameters and serum levels of soluble adhesion molecules of MS patients. Our data indicate that these TLR4 polymorphisms have no influence on the incidence, progression and inflammatory parameters of MS.

Alleles↗

PubMed1997

No linkage or association of a VNTR marker in the junction region of the immunoglobulin heavy chain genes in multiple sclerosis.

Multiple sclerosis (MS) is a demyelinating inflammatory disease of the central nervous system. Autoantibodies are though to participate in the pathogenesis. Previous reports on the role of immunoglobulin (Ig) variable gene segments in MS are contradictory. Here, by using a highly polymorphic variable number tandem repeat (VNTR) marker located in the centre of the IgH chain locus, we demonstrate a lack of linkage and association with MS in 34 multiplex families and 113 sporadic MS patients in Sweden. Stratification for the presence or absence of the MS-associated HLA-Dw2 haplotype did not influence the negative outcome. We conclude that the IgH chain genes are unlikely to play a role in genetic susceptibility to MS in the Swedish population.

Chromosomes, Human, Pair 14↗

PubMed2005

Nursing grand rounds: multiple sclerosis.

Multiple sclerosis (MS) is a highly variable, unpredictable disease and one of the most life-altering diagnoses a person can receive. Because it usually strikes in the prime of life, frequently progresses to disability, and has no cure, MS can make a strong emotional impact--not only on those who suffer from it, but also the healthcare team. Because MS is such a complex, multifaceted disorder, nurses who care for people with MS are faced with numerous clinical challenges. Many of the challenges are unique to MS, demanding, and time-consuming. Well-informed nurses are positioned to evaluate and explain the disease process, assist in the alleviation of symptoms, educate partners and families, and help improve quality of life. A case example can help nurses understand the real-life concerns of a person with MS.

Adult↗

PubMed1998

Seasonal variation of interferon-gamma production in progressive multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. There is increased interferon (IFN)-gamma secretion in MS patients in vitro, and IFN-gamma administration induces exacerbations of disease suggesting a link between IFN-gamma and disease activity. We observed significantly increased IFN-gamma production in the autumn and winter months compared with the spring and summer months in chronic progressive MS, and this increase was linked to endogenous interleukin (IL)-12 production. Increased seasonal IFN-gamma was not observed in normal control subjects, and there were no seasonal changes in IL-10 in progressive MS. These results suggest a potential environmental link between dysregulated IFN-gamma production and MS disease progression and pathogenesis.

Cells, Cultured↗

PubMed2006

The B cell response in multiple sclerosis.

Multiple sclerosis (MS) plaques and CSF contain increased amounts of intrathecally synthesized IgG, manifest as oligoclonal bands (OCBs) after protein electrophoresis. OCBs are not unique to MS and are also produced in infectious diseases of the CNS, in which the oligoclonal IgG has been shown to be antibody directed against the disease-causing agent. Thus, analysis of antibody specificity may identify the causative agent/antigen in MS. This review discusses recent studies that have analyzed the phenotypes of B cells in MS which infiltrate the CNS and the molecular features of their antigen-binding regions. Together with histologic studies showing the presence of ectopic lymphoid follicles in the meninges of some MS patients, this data supports the notion of a targeted and compartmentalized humoral response in MS.

Animals↗

PubMed2003

Genetic analysis of multiple sclerosis.

Multiple sclerosis (MS) is a complex disease with a significant genetic contribution. Similar to other complex diseases, the genetic risk for MS results from a combination of many genetic variants which individually confer only modest effects. Here we review the results of the complementary genetic approaches of linkage and association in MS, highlighting the challenges of identifying loci of modest effect. We describe meta-analytical approaches that provide additional statistical power necessary for detecting such loci and further apply this approach to evaluate the association of a CTLA-4 variant with MS. Lastly, we review recent important advances in our understanding of the patterns of genetic variation in the human genome and speculate about how these advances will aid in future studies of the genetic causes of MS.

Genetic Linkage↗

PubMed2000

[Recent progress in treatment for multiple sclerosis].

Multiple sclerosis (MS) is currently considered to be an autoimmune disease mediated by myelin antigen-specific Th 1 cells. Although the mechanism of MS remains to be elucidated, new disease modifying drugs have recently been introduced to MS treatment. Interferon-beta, copolymer 1 and intravenous administration of immunoglobulins have been shown to significantly reduce the relapse rate, progression of disease and increase of MRI lesion load in MS. However, as the effects of these drugs are nonspecific immunomodulation, specific immunomodulation therapy for MS is called for. T cell vaccination, altered peptide ligand and oral tolerance are possible candidates for specific immune therapy for MS. As in Asians there is such a distinct subtype of MS as HLA-DPB 1 * 0501-associated opticospinal MS, it is important to look for unique immune therapy for opticospinal MS in future.

Glatiramer Acetate↗

PubMed1987

[Alpha genes of the T cell receptor: a possible implication in genetic susceptibility to multiple sclerosis].

Multiple sclerosis (MS) is a neurological disease in which 60% of patients are DR2 (versus 20% in controls). Restriction fragment length polymorphism (RFLP) associated with T cell receptor alpha-chain and beta-chain genes have been analysed in a sample of 46 MS patients and compared with those of 142 controls. The alpha-chain gene polymorphism is localized to the V-J region and consists of 3 Bgl II alleles (alpha a = 3.2 kb; alpha b = 2.9 kb; alpha c = 2.8 kb). A significant difference was found in the distribution of these three alleles since 97% of DR2 patients versus 60% in DR2 non-MS individuals were found to be homozygotes alpha a/alpha a. These results suggest the influence of T cell antigen receptor germ line repertoire on the etiopathology of this disease.

Alleles↗

PubMed1999

Candidate autoantigens in multiple sclerosis.

Multiple sclerosis is an inflammatory demyelinating CNS disease of putatively autoimmune origin. Novel models of experimental autoimmune encephalomyelitis (EAE) have demonstrated that T cells specific for various myelin and even nonmyelin proteins are potentially encephalitogenic. The encephalitogenic T cell response directed against different CNS antigens not only determines the lesional topography of CNS inflammation but also the composition of the inflammatory infiltrates. The heterogeneity of the lesional distribution seen in EAE might therefore be useful for the understanding of the various clinical subtypes seen in MS. In this review the possible candidate autoantigens in MS are discussed with special regard to the human T cell and B cell responses against various myelin and nonmyelin proteins.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1994

Association of HLA and multiple sclerosis.

Multiple Sclerosis (MS) is a demyelinating disease of the central nervous system. Although the cause of MS is still unknown, it is considered an autoimmune disease based on the composition of inflammatory infiltrates in the brain and on parallels with a T-cell-mediated animal model of demyelinating diseases called experimental allergic encephalomyelitis (EAE). Similar to other autoimmune diseases, the immunogenetic background, in particular the MHC/HLA type, contributes to susceptibility. This review summarizes the current knowledge about the association between HLA background and MS as well as immunological findings in EAE and MS. Finally, an attempt is made to explain how structural interactions between disease-associated HLA type and binding of an autoantigenic peptide could relate to disease.

Alleles↗

PubMed1998

Genetics of multiple sclerosis.

Multiple sclerosis (MS) is a common demyelinating disease of the central nervous system affecting primarily young adults. Evidence from genetic epidemiological studies demonstrate that the observed familial clustering of MS is primarily due to shared genes between family members. Molecular investigations have failed to elucidate susceptibilty loci with the exception of the HLA DRB1*1501, DQA1*0102, DQB1*0602 haplotype of the major histocompatibility complex. Results from genomic screens stress the complexity of MS genetics and that there is no one single locus contributing significantly to familial risk. To overcome the confounding effects of genetic complexity, MS genetic research needs to take advantage of clinical and epidemiological information to better homogenize study samples. In addition, the continued collection and genotyping of MS families may shed some light on the mild to moderate susceptibility loci affecting the MS patient population.

Adoption↗

PubMed2006

Multiple sclerosis associated with systemic sclerosis.

Multiple sclerosis (MS) has been increasingly reported in association with other autoimmune diseases not primary affected the nervous system. The coexistence of MS and systemic sclerosis (SSc) has been rarely described. We report here the case of a 46-year-old female patient with longstanding MS since the age of 26, who developed SSc 12 years later. Her MS was of the relapsing-remitting type, but the definite diagnosis was not made until the age of 33. MS diagnosis was based on medical history, magnetic resonance imaging (MRI) studies and positive cerebrospinal fluid analysis. One year after the diagnosis of MS, she developed Raynaud's phenomenon, skin tightness and hypopigmented patches, suggestive of scleroderma. Further investigation with laboratory studies, including serology, hand and chest X-rays, and chest computerized tomography scan confirmed the SSc diagnosis. Our report highlights the interesting association between MS and SSc that may be due to an overlapping pathogenetic mechanism for both processes.

Adult↗

PubMed2000

Genetics of multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Although environmental risk factors are clearly involved in MS, the importance of genetic factors has been strongly supported by the results of studies on multiplex families, though a weak association with major histocompatibility complex (MHC) has been the only genetic feature of MS consistently observed to date. Other candidates genes have been pointed out, but none has been confirmed. Recent genome scans suggest that no single MS susceptibility locus is necessary or sufficient to cause MS, and this finding is compatible with a polygenic etiology. Furthermore, MS is a heterogeneous disorder, and thus different genes may influence its course or presentation. Actually, some candidate genes have been proposed, which contribute to the genotype-phenotype interactions in MS.

Cytokines↗

PubMed1985

Albumin and immunoglobulin-G in the cerebrospinal fluid and the diagnosis of multiple sclerosis.

Multiple sclerosis (MS) remains a diagnosis based mainly on clinical criteria. Definitive diagnostic tests are, despite numerous attempts, not available. However, some laboratory tests like electrophoresis of the cerebrospinal fluid proteins or the determination of immunoglobulin G in cerebrospinal fluid have proved useful in increasing the probability of MS. This paper describes how these laboratory tests have to be interpreted in relation to pathophysiological phenomena and how they correlate with each other. The electrophoresis of CSF proteins and the diagnostic quotients (Ralb and CSF-IgG-index) are valuable aids to the clinician. It especially can substantiate the diagnosis MS. The magnitude of the index cannot be correlated with the clinical stage of MS. The usefulness of these tests in terms of a possible gain of information in the diagnostic process is discussed.

Albumins↗

PubMedDate not supplied

[Neuropsychiatric and cognitive aspectos of multiple sclerosis].

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease that can affect cognitive and emotional functioning. About 50% of MS patients present some degree of neuropsychological impairment. Due to its onset in young adulthood (a period of life in which the individual is professionally and socially very active) the presence of cognitive impairment may greatly alter the patient's daily living activities and future life plans. Memory, attention, executive function and information processing speed are the most commonly reported impaired aspects of cognition. Depression, euphoria, and pathological laughing and crying are frequent psychiatric findings. In this paper we describe the distinctive features of cognitive and psychopathological impairments and their relationship to certain disease variables such as illness duration, lesion sites, physical impairment and clinical course. We also deal with aspects of the neuropsychological and psychiatric assessment, emphasizing its importance when psychological counseling or an eventual cognitive training are needed.

Cognition Disorders↗

PubMed2006

Search for genetic factors associated with susceptibility to multiple sclerosis.

Multiple sclerosis (MS) is a cell-mediated autoimmune disease characterized by type-1 cytokine production. Environmental and individual genetic background might influence this response particularly in cytokine gene polymorphisms. We evaluated whether polymorphisms of interleukin (IL)-10, IL-12, and tumor necrosis factor (TNF)-alpha genes, which might play a role in MS pathogenesis, are associated with MS susceptibility. Genotype frequencies for all the analyzed polymorphisms were not differently distributed between cases and controls. It is reasonable to suppose that the cytokine single-nucleotide polymorphisms (SNPs) studied must be considered against a larger genetic background involving other functional SNPs of Th1 regulator elements such as IL-21 and IL-23.

Case-Control Studies↗

PubMed2004

Increased CXCL8 (IL-8) expression in Multiple Sclerosis.

Multiple Sclerosis (MS) is a chronic inflammatory disease of the CNS which is characterized by large mononuclear cell infiltration and significant demyelination. CXCL8 is a chemo-attractant for both neutrophils and monocytes and triggers their firm adhesion to endothelium. In this study, we demonstrate that serum CXCL8 and CXCL8 secretion from PBMCs are significantly higher in untreated MS patients compared to controls and are significantly reduced in MS patients receiving interferon-beta1a therapy. We suggest that CXCL8 may serve as a marker of monocyte activity in MS and may play a role in monocyte recruitment to the CNS.

Adult↗