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[PMID]:28684532
[Au] Autor:Hyun JW; Woodhall MR; Kim SH; Jeong IH; Kong B; Kim G; Kim Y; Park MS; Irani SR; Waters P; Kim HJ
[Ad] Endereço:Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Korea.
[Ti] Título:Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases.
[So] Source:J Neurol Neurosurg Psychiatry;88(10):811-817, 2017 Oct.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We evaluated the seroprevalence of myelin oligodendrocyte glycoprotein immunoglobulin G1 (MOG-IgG) and associated clinical features of patients from a large adult-dominant unselected cohort with mainly relapsing central nervous system (CNS) inflammatory diseases. We also investigate the clinical relevance of MOG-IgG through a longitudinal analysis of serological status over a 2-year follow-up period. METHODS: Serum samples from 505 patients with CNS inflammatory diseases at the National Cancer Center were analysed using cell-based assays for MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG). MOG-IgG serostatus was longitudinally assessed in seropositive patients with available serum samples and at least 2 years follow-up. RESULTS: Twenty-two of 505 (4.4%) patients with CNS inflammatory diseases were positive for MOG-IgG. Patients with MOG-IgG had neuromyelitis optica spectrum disorder (NMOSD, n=10), idiopathic AQP4-IgG-negative myelitis (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3) and multiple sclerosis (n=1). No relapses were seen in patients when they became MOG-IgG seronegative, whereas a persistent positive serological status was observed in patients with clinical relapses despite immunotherapy. CONCLUSIONS: In a large adult-predominant unselected cohort of mainly relapsing CNS inflammatory diseases, we confirmed that NMOSD phenotype was most commonly observed in patients with MOG-IgG. A longitudinal analysis with 2-year follow-up suggested that persistence of MOG-IgG is associated with relapses.
[Mh] Termos MeSH primário: Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central
Glicoproteína Mielina-Oligodendrócito/imunologia
Estudos Soroepidemiológicos
[Mh] Termos MeSH secundário: Aquaporina 4/imunologia
Autoanticorpos/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/sangue
Seres Humanos
Imunoglobulina G/sangue
Estudos Longitudinais
Imagem por Ressonância Magnética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 4); 0 (Autoantibodies); 0 (Immunoglobulin G); 0 (Myelin-Oligodendrocyte Glycoprotein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2017-315998


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[PMID]:28473042
[Au] Autor:Chaudhry HM; Mauermann ML; Rajkumar SV
[Ad] Endereço:Mayo Clinic School of Medicine, Mayo Clinic, Rochester, MN.
[Ti] Título:Monoclonal Gammopathy-Associated Peripheral Neuropathy: Diagnosis and Management.
[So] Source:Mayo Clin Proc;92(5):838-850, 2017 May.
[Is] ISSN:1942-5546
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Monoclonal gammopathies comprise a spectrum of clonal plasma cell disorders that include monoclonal gammopathy of undetermined significance, multiple myeloma, and Waldenström macroglobulinemia. In this review, we outline the epidemiology, etiology, classification, diagnosis, and treatment of monoclonal gammopathy-associated peripheral neuropathy. Monoclonal gammopathy of undetermined significance is relatively common in the general population, with a prevalence of 3% to 4% among individuals older than age 50 years. Therefore, the presence of M protein in a patient with neuropathy does not automatically indicate a causal relationship. Monoclonal gammopathy-associated peripheral neuropathy is often a difficult diagnosis with limited treatment options. Studies addressing the optimal approach to diagnosis and management of this entity are limited. In addition to a review of the literature, we present a diagnostic approach to patients with monoclonal gammopathy-associated peripheral neuropathy and discuss available data and options for treatment.
[Mh] Termos MeSH primário: Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/diagnóstico
Glicoproteínas/análise
Imunoglobulinas/administração & dosagem
Gamopatia Monoclonal de Significância Indeterminada/complicações
Doenças do Sistema Nervoso Periférico/diagnóstico
Plasmaferese/métodos
Rituximab/uso terapêutico
Vidarabina/análogos & derivados
[Mh] Termos MeSH secundário: Administração Intravenosa
Biomarcadores/análise
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/epidemiologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/etiologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/imunologia
Diagnóstico Diferencial
Glicoproteínas/efeitos adversos
Seres Humanos
Fatores Imunológicos/uso terapêutico
Gamopatia Monoclonal de Significância Indeterminada/epidemiologia
Gamopatia Monoclonal de Significância Indeterminada/imunologia
Agonistas Mieloablativos/uso terapêutico
Doenças do Sistema Nervoso Periférico/epidemiologia
Doenças do Sistema Nervoso Periférico/etiologia
Doenças do Sistema Nervoso Periférico/terapia
Prognóstico
Vidarabina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycoproteins); 0 (Immunoglobulins); 0 (Immunologic Factors); 0 (Myeloablative Agonists); 0 (protein M (glycoprotein)); 4F4X42SYQ6 (Rituximab); FA2DM6879K (Vidarabine); P2K93U8740 (fludarabine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


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[PMID]:28381515
[Au] Autor:Aubert-Broche B; Weier K; Longoni G; Fonov VS; Bar-Or A; Marrie RA; Yeh EA; Narayanan S; Arnold DL; Verhey LH; Banwell B; Collins DL; Canadian Pediatric Demyelinating Disease Network
[Ad] Endereço:From the McConnell Brain Imaging Center (B.A.-B., K.W., V.S.F., S.N., D.L.A., D.L.C.) and Department of Neurology and Neurosurgery and Experimental Therapeutics Program (A.B.-O.), Montreal Neurological Institute, McGill University; The Hospital for Sick Children (G.L., E.A.Y., L.H.V.), University of
[Ti] Título:Monophasic demyelination reduces brain growth in children.
[So] Source:Neurology;88(18):1744-1750, 2017 May 02.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate how monophasic acquired demyelinating syndromes (ADS) affect age-expected brain growth over time. METHODS: We analyzed 83 pediatric patients imaged serially from initial demyelinating attack: 18 with acute disseminated encephalomyelitis (ADEM) and 65 with other monophasic ADS presentations (monoADS). We further subdivided the monoADS group by the presence (n = 33; monoADSlesion) or absence (n = 32; monoADSnolesion) of T2 lesions involving the brain at onset. We used normative data to compare brain volumes and calculate age- and sex-specific scores, and used mixed-effect models to investigate their relationship with time from demyelinating illness. RESULTS: Children with monophasic demyelination (ADEM, non-ADEM with brain lesions, and those without brain involvement) demonstrated reduced age-expected brain growth on serial images, driven by reduced age-expected white matter growth. Cortical gray matter volumes were not reduced at onset but demonstrated reduced age-expected growth afterwards in all groups. Brain volumes differed from age- and sex-expected values to the greatest extent in children with ADEM. All patient groups failed to recover age-expected brain growth trajectories. CONCLUSIONS: Brain volume, and more importantly age-expected brain growth, is negatively affected by acquired demyelination, even in the absence of chronicity, implicating factors other than active inflammation as operative in this process.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Encéfalo/crescimento & desenvolvimento
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Feminino
Seguimentos
Substância Cinzenta/diagnóstico por imagem
Substância Cinzenta/crescimento & desenvolvimento
Seres Humanos
Estudos Longitudinais
Imagem por Ressonância Magnética
Masculino
Tamanho do Órgão
Estudos Prospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170526
[Lr] Data última revisão:
170526
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003884


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[PMID]:28284341
[Au] Autor:Zhou L; Huang Y; Li H; Fan J; Zhangbao J; Yu H; Li Y; Lu J; Zhao C; Lu C; Wang M; Quan C
[Ad] Endereço:Department of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, China.
[Ti] Título:MOG-antibody associated demyelinating disease of the CNS: A clinical and pathological study in Chinese Han patients.
[So] Source:J Neuroimmunol;305:19-28, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We aim to evaluate the clinical relevance of MOG-ab in a cohort of Chinese Han adults with CNS inflammatory demyelinating diseases (IDDs). MOG-ab and AQP4-ab were examined through a fixed cell based indirect immune-fluorescence assay in 86 patients with CNS-IDDs. MOG-ab was positive in 12 patients, while AQP4-ab was positive in 31 patients; none double positives. Optic neuritis (ON) was the most frequent symptom at onset (75.0%) or during the whole disease course (83.3%) of MOG-ab associated IDDs (MOG-IDDs); 79.5% of the episodes involved only the optic nerve in MOG-IDDs. MOG-ab related ON (MOG-ON) usually caused severe visual impairment, longitudinally extensive optic nerve lesion with anterior enhancement and perineural soft tissue enhancement, responded well to steroid, but still could leave remarkable thinning of retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC). MOG-IDDs had less spinal cord involvement compared to AQP4-ab mediated NMO/SD. Heterogeneous brain lesions existed in 66.7% of the patients with MOG-IDDs. Large, edematous white matter lesions were observed with the pathological feature of obvious demyelination yet preservation of astrocyte and axon, fundamentally different from the astrocytopathy typically seen in NMO/SD. Our investigations suggest that MOG-ab mediates a distinct disease entity separate from NMO/SD.
[Mh] Termos MeSH primário: Aquaporina 4/imunologia
Autoanticorpos/sangue
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/patologia
Glicoproteína Mielina-Oligodendrócito/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Grupo com Ancestrais do Continente Asiático/etnologia
Encéfalo/diagnóstico por imagem
Criança
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/sangue
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/fisiopatologia
Ensaio de Imunoadsorção Enzimática
Olho/patologia
Feminino
Seres Humanos
Processamento de Imagem Assistida por Computador
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Retina/patologia
Medula Espinal/diagnóstico por imagem
Estatísticas não Paramétricas
Acuidade Visual
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP4 protein, human); 0 (Aquaporin 4); 0 (Autoantibodies); 0 (Myelin-Oligodendrocyte Glycoprotein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


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[PMID]:28283103
[Au] Autor:Abdullah S; Fadzli F; Ramli N; Tan CT
[Ad] Endereço:Department of Medicine, University Malaya Medical Centre, Kuala Lumpur, Malaysia. Electronic address: suhailahabd08@yahoo.com.
[Ti] Título:There is less MRI brain lesions and no characteristic MRI Brain findings in IIDDs patients with positive AQP4 serology among Malaysians.
[So] Source:Mult Scler Relat Disord;12:34-38, 2017 Feb.
[Is] ISSN:2211-0356
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: The recently introduced International Consensus diagnostic criteria for diagnosis of neuromyelitis spectrum disorder include patients who are seronegative for AQP4 antibody. The criteria are dependent on typical MRI changes in the spinal cord, optic nerve and brain. This study aims to determine whether there are significant differences in the MRI brain images between AQP4 positive and negative patients with IIDDs. METHOD: MRI brain of patients with a diagnosis of IIDDs presented to the Hospital from 2010 to 2015 was analysed. The MRI was assessed by 2 radiologists blinded to the AQP4 status, on features said to be typical of NMOSD and MS. RESULTS: Thirty nine patients fulfilled the criteria and were included in the study. They consisted of 19 AQP4 seropositive and 20 AQP4 seronegative patients. The mean age was older (37.0 vs. 28.8 years) among the AQP4 positive group. The majority of the patients were ethnic Chinese (72%), followed by the Malays and Indians. Those with AQP4 seropositive status generally has less brain lesions, and significantly less fulfilling the McDonald DIS criteria as compared to those with AQP4 seronegative status (15.8% vs. 60.0%, p=0.005). None of the seven cerebral MRI features highlighted in NMOSD 2015 diagnostic criteria, said to be characteristic of NMOSD was more common among the AQP4 positive patients. These features were in fact seen less frequently among the AQP4 seropositive patients. An example was the extensive hemispheric lesion seen in 10.5% of AQP4 seropositive patients vs. 45% of that AQP4 seronegative group. CONCLUSION: There was no characteristic MRI brain features in the Malaysian AQP4 seropositive IIDD patients versus those who are seronegative. This could be a reflection of ethnical difference.
[Mh] Termos MeSH primário: Aquaporina 4/sangue
Encéfalo/diagnóstico por imagem
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/sangue
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/diagnóstico por imagem
Imagem por Ressonância Magnética
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Feminino
Seres Humanos
Malásia
Masculino
Estudos Retrospectivos
Método Simples-Cego
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP4 protein, human); 0 (Aquaporin 4); 0 (Biomarkers)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170320
[Lr] Data última revisão:
170320
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE


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[PMID]:28220542
[Au] Autor:Tremlett H; Bauer KC; Appel-Cresswell S; Finlay BB; Waubant E
[Ad] Endereço:Faculty of Medicine (Neurology) and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:The gut microbiome in human neurological disease: A review.
[So] Source:Ann Neurol;81(3):369-382, 2017 Mar.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Almost half the cells and 1% of the unique genes found in our bodies are human, the rest are from microbes, predominantly bacteria, archaea, fungi, and viruses. These microorganisms collectively form the human microbiota, with most colonizing the gut. Recent technological advances, open access data libraries, and application of high-throughput sequencing have allowed these microbes to be identified and their contribution to neurological health to be examined. Emerging evidence links perturbations in the gut microbiota to neurological disease, including disease risk, activity, and progression. This review provides an overview of the recent advances in microbiome research in relation to neuro(auto)immune and neurodegenerative conditions affecting humans, such as multiple sclerosis, neuromyelitis optica spectrum disorders, Parkinson disease, Alzheimer disease, Huntington disease, and amyotrophic lateral sclerosis. Study design and terminology used in this rapidly evolving, highly multidisciplinary field are summarized to empower and engage the neurology community in this "newly discovered organ." Ann Neurol 2017;81:369-382.
[Mh] Termos MeSH primário: Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central
Microbioma Gastrointestinal/fisiologia
Doenças Neurodegenerativas
[Mh] Termos MeSH secundário: Animais
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/etiologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/microbiologia
Seres Humanos
Doenças Neurodegenerativas/etiologia
Doenças Neurodegenerativas/imunologia
Doenças Neurodegenerativas/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24901


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[PMID]:28131219
[Au] Autor:Doneddu PE; Kazmi M; Samuel M; Mahdi-Rogers M; Hadden RD
[Ad] Endereço:Department of Neurology, King's College Hospital, King's College London, Denmark Hill, SE5 9RS London, UK. Electronic address: pietro.e.doneddu@gmail.com.
[Ti] Título:Deterioration of tremor after treatment with rituximab in anti-MAG neuropathy.
[So] Source:J Neurol Sci;373:344-345, 2017 Feb 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/tratamento farmacológico
Fatores Imunológicos/efeitos adversos
Glicoproteína Associada a Mielina/imunologia
Paraproteinemias/tratamento farmacológico
Rituximab/efeitos adversos
Tremor/etiologia
[Mh] Termos MeSH secundário: Idoso
Autoanticorpos/metabolismo
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/fisiopatologia
Avaliação da Deficiência
Seres Humanos
Imunoglobulina M/metabolismo
Fatores Imunológicos/uso terapêutico
Masculino
Paraproteinemias/fisiopatologia
Rituximab/uso terapêutico
Índice de Gravidade de Doença
Tremor/fisiopatologia
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Immunoglobulin M); 0 (Immunologic Factors); 0 (MAG protein, human); 0 (Myelin-Associated Glycoprotein); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:28069755
[Au] Autor:Colpitts SL; Kasper LH
[Ad] Endereço:Department of Microbiology and Immunology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755 sara.l.colpitts@dartmouth.edu.
[Ti] Título:Influence of the Gut Microbiome on Autoimmunity in the Central Nervous System.
[So] Source:J Immunol;198(2):596-604, 2017 Jan 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoimmune disorders of the CNS have complex pathogeneses that are not well understood. In multiple sclerosis and neuromyelitis optica spectrum disorders, T cells destroy CNS tissue, resulting in severe disabilities. Mounting evidence suggests that reducing inflammation in the CNS may start with modulation of the gut microbiome. The lymphoid tissues of the gut are specialized for the induction of regulatory cells, which are directly responsible for the suppression of CNS-damaging autoreactive T cells. Whether cause or effect, the onset of dysbiosis in the gut of patients with multiple sclerosis and neuromyelitis optica provides evidence of communication along the gut-brain axis. Thus, current and future therapeutic interventions directed at microbiome modulation are of considerable appeal.
[Mh] Termos MeSH primário: Autoimunidade/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/microbiologia
Microbioma Gastrointestinal/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601438


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[PMID]:28063151
[Au] Autor:McKeon A; Tracy JA
[Ad] Endereço:Department of Neurology, College of Medicine, Mayo Clinic, 200 1st Street SW, Rochester, Minnesota, 55905, USA.
[Ti] Título:GAD65 neurological autoimmunity.
[So] Source:Muscle Nerve;56(1):15-27, 2017 Jul.
[Is] ISSN:1097-4598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The glutamic acid decarboxylase 65-kilodalton isoform (GAD65) antibody is a biomarker of autoimmune central nervous system (CNS) disorders and, more commonly, nonneurological autoimmune diseases. Type 1 diabetes, autoimmune thyroid disease, and pernicious anemia are the most frequent GAD65 autoimmune associations. One or more of these disorders coexists in approximately 70% of patients with GAD65 neurological autoimmunity. Neurological phenotypes have CNS localization and include limbic encephalitis, epilepsy, cerebellar ataxia, and stiff-person syndrome (SPS), among others. Classic SPS is a disorder on the spectrum of CNS hyperexcitability which also includes phenotypes that are either more restricted (stiff-limb syndrome) or more widespread (progressive encephalomyelitis with rigidity and myoclonus). GAD65 antibody is not highly predictive of a paraneoplastic cause for neurological disorders, but diverse cancer types have been occasionally reported. For all phenotypes, responses to immunotherapy are variable (approximately 50% improve). GAD65 autoimmunity is important to recognize for both coexisting nonneurological autoimmune associations and potential immunotherapy-response. Muscle Nerve 56: 15-27, 2017.
[Mh] Termos MeSH primário: Autoanticorpos/metabolismo
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/metabolismo
Glutamato Descarboxilase/imunologia
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/imunologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1002/mus.25565


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[PMID]:28049030
[Au] Autor:Daneshdoust D; Khalili-Fomeshi M; Ghasemi-Kasman M; Ghorbanian D; Hashemian M; Gholami M; Moghadamnia A; Shojaei A
[Ad] Endereço:Student Research Committee, Faculty of Medical Sciences, Babol University of Medical Sciences, Babol, Mazandaran, Iran.
[Ti] Título:Pregabalin enhances myelin repair and attenuates glial activation in lysolecithin-induced demyelination model of rat optic chiasm.
[So] Source:Neuroscience;344:148-156, 2017 Mar 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple sclerosis (MS) is an autoimmune disease in which more than 70% of patients experience visual disturbance as the earliest symptoms. Lysolecithin (LPC)-induced focal demyelination model has been developed to evaluate the effects of different therapies on myelin repair improvement. In this study, the effects of pregabalin administration on myelin repair and glial activation were investigated. Local demyelination was induced by administration of LPC (1%, 2µL) into the rat optic chiasm. Rats underwent daily injection of pregabalin (30mg/kg, i.p) or vehicle. Visual-evoked potentials (VEPs) recordings were performed for evaluating the function of optic pathway on days 3, 7, 14 and 28 post lesions. Myelin specific staining and immunostaining against GFAP and Iba1 were also carried out for assessment of myelination and glial activation respectively. Electrophysiological data indicated that pregabalin administration could significantly reduce the P1-N1 latency and increase the amplitude of VEPs waves compared to saline group. Luxol fast blue staining and immunostaining against PLP, as mature myelin marker, showed that myelin repair was improved in animals received pregabalin treatment. In addition, pregabalin effectively reduced the expression of GFAP and Iba1 as activated glial markers in optic chiasm. The present study indicates that pregabalin administration enhances myelin repair and ameliorates glial activation of optic chiasm following local injection of LPC.
[Mh] Termos MeSH primário: Bainha de Mielina/efeitos dos fármacos
Doença Autoimune do Sistema Nervoso Experimental/tratamento farmacológico
Neuroglia/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Quiasma Óptico/efeitos dos fármacos
Pregabalina/farmacologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/metabolismo
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/tratamento farmacológico
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/patologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/fisiopatologia
Potenciais Evocados Visuais/efeitos dos fármacos
Proteína Glial Fibrilar Ácida/metabolismo
Lisofosfatidilcolinas
Masculino
Proteínas dos Microfilamentos/metabolismo
Bainha de Mielina/patologia
Bainha de Mielina/fisiologia
Doença Autoimune do Sistema Nervoso Experimental/patologia
Doença Autoimune do Sistema Nervoso Experimental/fisiopatologia
Neuroglia/patologia
Neuroglia/fisiologia
Quiasma Óptico/patologia
Quiasma Óptico/fisiopatologia
Distribuição Aleatória
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Glial Fibrillary Acidic Protein); 0 (Lysophosphatidylcholines); 0 (Microfilament Proteins); 0 (Neuroprotective Agents); 0 (glial fibrillary acid protein, rat); 55JG375S6M (Pregabalin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE



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