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[PMID]:27778395
[Au] Autor:Michailidou I; Naessens DM; Hametner S; Guldenaar W; Kooi EJ; Geurts JJ; Baas F; Lassmann H; Ramaglia V
[Ad] Endereço:Department of Genome Analysis, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105, The Netherlands.
[Ti] Título:Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease pathogenesis.
[So] Source:Glia;65(2):264-277, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglial clusters with C3d deposits are observed in the periplaque of multiple sclerosis (MS) brains and were proposed as early stage of lesion formation. As such they should appear in the brain of MS donors with acute disease but thus far this has not been shown. Using postmortem brain tissue from acute (n = 10) and chronic (n = 15) MS cases we investigated whether C3d+ microglial clusters are part of an acute attack against myelinated axons, which could have implications for disease pathogenesis. The specificity of our findings to MS was tested in ischemic stroke cases (n = 8) with initial or advanced lesions and further analyzed in experimental traumatic brain injury (TBI, n = 26), as both conditions are primarily nondemyelinating but share essential features of neurodegeneration with MS lesions. C3d+ microglial clusters were found in chronic but not acute MS. They were not associated with antibody deposits or terminal complement activation. They were linked to slowly expanding lesions, localized on axons with impaired transport and associated with neuronal C3 production. C3d+ microglial clusters were not specific to MS as they were also found in stroke and experimental TBI. We conclude that C3d+ microglial clusters in MS are not part of an acute attack against myelinated axons. As such it is unlikely that they drive formation of new lesions but could represent a physiological mechanism to remove irreversibly damaged axons in chronic disease. GLIA 2017;65:264-277.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Microglia/metabolismo
Esclerose Múltipla/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Autopsia
Doença Crônica
Complemento C3/genética
Citocinas/metabolismo
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Feminino
Traumatismos Cranianos Fechados/patologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Proteínas da Mielina/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/patologia
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (C3 protein, human); 0 (Complement C3); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (Myelin Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23090


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[PMID]:28980804
[Au] Autor:Hutchison JM; Lu Z; Li GC; Travis B; Mittal R; Deatherage CL; Sanders CR
[Ad] Endereço:Department of Biochemistry, Vanderbilt University School of Medicine , Nashville, Tennessee 37240, United States.
[Ti] Título:Dodecyl-ß-melibioside Detergent Micelles as a Medium for Membrane Proteins.
[So] Source:Biochemistry;56(41):5481-5484, 2017 Oct 17.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There remains a need for new non-ionic detergents that are suitable for use in biochemical and biophysical studies of membrane proteins. Here we explore the properties of n-dodecyl-ß-melibioside (ß-DDMB) micelles as a medium for membrane proteins. Melibiose is d-galactose-α(1→6)-d-glucose. Light scattering showed the ß-DDMB micelle to be roughly 30 kDa smaller than micelles formed by the commonly used n-dodecyl-ß-maltoside (ß-DDM). ß-DDMB stabilized diacylglycerol kinase (DAGK) against thermal inactivation. Moreover, activity assays conducted using aliquots of DAGK purified into ß-DDMB yielded activities that were 40% higher than those of DAGK purified into ß-DDM. ß-DDMB yielded similar or better TROSY-HSQC NMR spectra for two single-pass membrane proteins and the tetraspan membrane protein peripheral myelin protein 22. ß-DDMB appears be a useful addition to the toolbox of non-ionic detergents available for membrane protein research.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Detergentes/química
Diacilglicerol Quinase/metabolismo
Dissacarídeos/química
Proteínas de Escherichia coli/metabolismo
Glicolipídeos/química
Proteínas da Mielina/metabolismo
Receptor Notch1/metabolismo
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/química
Detergentes/síntese química
Diacilglicerol Quinase/química
Dissacarídeos/síntese química
Difusão Dinâmica da Luz
Estabilidade Enzimática
Proteínas de Escherichia coli/química
Glucosídeos/química
Glicolipídeos/síntese química
Temperatura Alta/efeitos adversos
Seres Humanos
Micelas
Proteínas da Mielina/química
Ressonância Magnética Nuclear Biomolecular
Tamanho da Partícula
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Estabilidade Proteica
Receptor Notch1/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APP protein, human); 0 (Amyloid beta-Protein Precursor); 0 (Detergents); 0 (Disaccharides); 0 (Escherichia coli Proteins); 0 (Glucosides); 0 (Glycolipids); 0 (Micelles); 0 (Myelin Proteins); 0 (NOTCH1 protein, human); 0 (PMP22 protein, human); 0 (Peptide Fragments); 0 (Receptor, Notch1); 0 (dodecyl-beta-melibioside); 69227-93-6 (dodecyl maltoside); EC 2.7.1.107 (Diacylglycerol Kinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00810


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[PMID]:28807492
[Au] Autor:Lei HW; Wang JY; Dang QJ; Yang F; Liu X; Zhang JH; Li Y
[Ad] Endereço:Department of Rheumatology and Immunology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, PR China.
[Ti] Título:Neuropsychiatric involvement in lupus is associated with the Nogo-a/NgR1 pathway.
[So] Source:J Neuroimmunol;311:22-28, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuroinflammation- and neurodegeneration-induced nerve injury may represent important components of neuropsychiatric lupus (NPSLE). Myelin-associated neurite outgrowth inhibitor (Nogo)-a and its receptor, NgR1, limit recovery of the adult central nervous system after injury. We detected a soluble Nogo-a product in the cerebral spinal fluid of patients with NPSLE. In a mouse model of lupus, aging was associated with an increase in Nogo-a positive neurons, diminished myelin sheaths, enhanced pro-inflammatory cytokines, and impaired cognition and memory. Treatment with the Nogo-66 antagonist promoted myelin repair, improved cognition and memory, and downregulated pro-inflammatory factors. Our data imply the Nogo-a/NgR1 pathway is involved in NPSLE.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Vasculite Associada ao Lúpus do Sistema Nervoso Central/metabolismo
Vasculite Associada ao Lúpus do Sistema Nervoso Central/patologia
Proteínas Nogo/metabolismo
Receptor Nogo 1/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Adulto
Animais
Encéfalo/patologia
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Feminino
Seres Humanos
Vasculite Associada ao Lúpus do Sistema Nervoso Central/tratamento farmacológico
Vasculite Associada ao Lúpus do Sistema Nervoso Central/genética
Masculino
Aprendizagem em Labirinto/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Meia-Idade
Proteínas da Mielina/uso terapêutico
Neurônios/metabolismo
Proteínas Nogo/genética
Receptor Nogo 1/genética
Fragmentos de Peptídeos/uso terapêutico
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Myelin Proteins); 0 (NEP1-40 protein, human); 0 (Nogo Proteins); 0 (Nogo Receptor 1); 0 (Peptide Fragments)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28796392
[Au] Autor:Cornett KMD; Menezes MP; Shy RR; Moroni I; Pagliano E; Pareyson D; Estilow T; Yum SW; Bhandari T; Muntoni F; Laura M; Reilly MM; Finkel RS; Eichinger KJ; Herrmann DN; Bray P; Halaki M; Shy ME; Burns J; CMTPedS Study Group
[Ad] Endereço:The University of Sydney, Sydney Children's Hospitals Network (Randwick and Westmead, Sydney, New South Wales, Australia.
[Ti] Título:Natural history of Charcot-Marie-Tooth disease during childhood.
[So] Source:Ann Neurol;82(3):353-359, 2017 Sep.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine the rate of disease progression in a longitudinal natural history study of children with Charcot-Marie-Tooth (CMT) disease. METHODS: Two hundred six (103 female) participants aged 3 to 20 years enrolled in the Inherited Neuropathies Consortium were assessed at baseline and 2 years. Demographic, anthropometric, and diagnostic information were collected. Disease progression was assessed with the CMT Pediatric Scale (CMTPedS), a reliable Rasch-built linearly weighted disability scale evaluating fine and gross motor function, strength, sensation, and balance. RESULTS: On average, CMTPedS Total scores progressed at a rate of 2.4 ± 4.9 over 2 years (14% change from baseline; p < 0.001). There was no difference between males and females (mean difference, 0.5; 95% confidence interval [CI], -0.9 to 1.9; p = 0.49). The most responsive CMTPedS items were dorsiflexion strength (z-score change, -0.3; 95% CI, -0.6 to -0.05; p = 0.02), balance (z-score change, -1.0; 95% CI, -1.9 to -0.09; p = 0.03), and long jump (z-score change, -0.4; 95% CI, -0.7 to -0.02; p = 0.04). Of the most common genetic subtypes, 111 participants with CMT1A/PMP22 duplication progressed by 1.8 ± 4.2 (12% change from baseline; p < 0.001), 9 participants with CMT1B/MPZ mutation progressed by 2.2 ± 5.1 (11% change), 6 participants with CMT2A/MFN2 mutation progressed by 6.2 ± 7.9 (23% change), and 7 participants with CMT4C/SH3TC2 mutations progressed by 3.0 ± 4.5 (12% change). Participants with CMT2A progressed faster than CMT1A (mean difference, -4.4; 95% CI, -8.1 to -0.8; p = 0.02). Children with CMT1A progressed consistently through early childhood (3-10 years) and adolescence (11-20 years; mean difference, 1.1; 95% CI, -0.6 to 2.7; p = 0.19), whereas CMT2A appeared to progress faster during early childhood than adolescence (mean difference, 10.0; 95% CI, -2.2 to 22.2; p = 0.08). INTERPRETATION: Using the CMTPedS as an outcome measure of disease severity, children with CMT progress at a significant rate over 2 years. Understanding the rate at which children with CMT deteriorate is essential for adequately powering trials of disease-modifying interventions. Ann Neurol 2017;82:353-359.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/patologia
[Mh] Termos MeSH secundário: Adolescente
Doença de Charcot-Marie-Tooth/genética
Criança
Pré-Escolar
Progressão da Doença
Feminino
Seres Humanos
Estudos Longitudinais
Masculino
Mutação
Proteínas da Mielina/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myelin Proteins); 0 (PMP22 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1002/ana.25009


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[PMID]:28341461
[Au] Autor:Chen K; Marsh BC; Cowan M; Al'Joboori YD; Gigout S; Smith CC; Messenger N; Gamper N; Schwab ME; Ichiyama RM
[Ad] Endereço:School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom; School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China.
[Ti] Título:Sequential therapy of anti-Nogo-A antibody treatment and treadmill training leads to cumulative improvements after spinal cord injury in rats.
[So] Source:Exp Neurol;292:135-144, 2017 Jun.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intense training is the most clinically successful treatment modality following incomplete spinal cord injuries (SCIs). With the advent of plasticity enhancing treatments, understanding how treatments might interact when delivered in combination becomes critical. Here, we investigated a rational approach to sequentially combine treadmill locomotor training with antibody mediated suppression of the fiber growth inhibitory protein Nogo-A. Following a large but incomplete thoracic lesion, rats were immediately treated with either anti-Nogo-A or control antibody (2weeks) and then either left untrained or step-trained starting 3weeks after injury for 8weeks. It was found that sequentially combined therapy improved step consistency and reduced toe dragging and climbing errors, as seen with training and anti-Nogo-A individually. Animals with sequential therapy also adopted a more parallel paw position during bipedal walking and showed greater overall quadrupedal locomotor recovery than individual treatments. Histologically, sequential therapy induced the greatest corticospinal tract sprouting caudally into the lumbar region and increased the number of serotonergic synapses onto lumbar motoneurons. Increased primary afferent sprouting and synapse formation onto lumbar motoneurons observed with anti-Nogo-A antibody were reduced by training. Animals with sequential therapy also showed the highest reduction of lumbar interneuronal activity associated with walking (c-fos expression). No treatment effects for thermal nociception, mechanical allodynia, or lesion volume were observed. The results demonstrate that sequential administration of anti-Nogo-A antibody followed in time with intensive locomotor training leads to superior recovery of lost locomotor functions, which is probably mediated by changes in the interaction between descending sprouting and local segmental networks after SCI.
[Mh] Termos MeSH primário: Anticorpos/farmacologia
Locomoção/efeitos dos fármacos
Regeneração Nervosa/efeitos dos fármacos
Tratos Piramidais/efeitos dos fármacos
Recuperação de Função Fisiológica/efeitos dos fármacos
Traumatismos da Medula Espinal/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Feminino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Proteínas da Mielina/metabolismo
Plasticidade Neuronal/efeitos dos fármacos
Plasticidade Neuronal/fisiologia
Proteínas Nogo/imunologia
Proteínas Nogo/metabolismo
Condicionamento Físico Animal
Ratos Sprague-Dawley
Recuperação de Função Fisiológica/fisiologia
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Myelin Proteins); 0 (Nogo Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE


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[PMID]:28340598
[Au] Autor:Liu Y; Given KS; Harlow DE; Matschulat AM; Macklin WB; Bennett JL; Owens GP
[Ad] Endereço:Department of Neurology, University of Colorado, School of Medicine, 12700 E. 19th Ave, Aurora, CO, USA.
[Ti] Título:Myelin-specific multiple sclerosis antibodies cause complement-dependent oligodendrocyte loss and demyelination.
[So] Source:Acta Neuropathol Commun;5(1):25, 2017 Mar 24.
[Is] ISSN:2051-5960
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intrathecal immunoglobulin G (IgG) synthesis, cerebrospinal fluid (CSF) oligoclonal IgG bands and lesional IgG deposition are seminal features of multiple sclerosis (MS) disease pathology. Both the specific targets and pathogenic effects of MS antibodies remain poorly characterized. We produced IgG1 monoclonal recombinant antibodies (rAbs) from clonally-expanded plasmablasts recovered from MS patient CSF. Among these were a subset of myelin-specific MS rAbs. We examined their immunoreactivity to mouse organotypic cerebellar slices by live binding and evaluated tissue injury in the presence and absence of human complement. Demyelination, glial and neuronal viability, and complement pathway activation were assayed by immunofluorescence microscopy and compared to the effects of an aquaporin-4 water channel (AQP4)-specific rAb derived from a neuromyelitis optica (NMO) patient. MS myelin-specific rAbs bound to discrete surface domains on oligodendrocyte processes and myelinating axons. Myelin-specific MS rAbs initiated complement-dependent cytotoxicity to oligodendrocytes and induced rapid demyelination. Demyelination was accompanied by increased microglia activation; however, the morphology and survival of astrocytes, oligodendrocyte progenitors and neurons remained unaffected. In contrast, NMO AQP4-specific rAb initiated complement-dependent astrocyte damage, followed by sequential loss of oligodendrocytes, demyelination, microglia activation and neuronal death. Myelin-specific MS antibodies cause oligodendrocyte loss and demyelination in organotypic cerebellar slices, which are distinct from AQP4-targeted pathology, and display seminal features of active MS lesions. Myelin-specific antibodies may play an active role in MS lesion formation through complement-dependent mechanisms.
[Mh] Termos MeSH primário: Proteínas do Sistema Complemento/imunologia
Imunoglobulina G/imunologia
Esclerose Múltipla/imunologia
Proteínas da Mielina/imunologia
Oligodendroglia/imunologia
Oligodendroglia/patologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/imunologia
Astrócitos/patologia
Morte Celular
Cerebelo/imunologia
Cerebelo/patologia
Proteínas do Sistema Complemento/metabolismo
Seres Humanos
Imunoglobulina G/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microglia/imunologia
Microglia/patologia
Esclerose Múltipla/patologia
Neurônios/imunologia
Neurônios/patologia
Neurite Óptica/imunologia
Neurite Óptica/patologia
Plasmócitos/imunologia
Proteínas Recombinantes/metabolismo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Myelin Proteins); 0 (Recombinant Proteins); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE
[do] DOI:10.1186/s40478-017-0428-6


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[PMID]:28315720
[Au] Autor:Hao GM; Liu YG; Wu Y; Xing W; Guo SZ; Wang Y; Wang ZL; Li C; Lv TT; Wang HL; Shi TJ; Wang W; Han J
[Ad] Endereço:College of Basic Medicine, Key Laboratory of Ministry of Education (Syndromes and Formulas), Key Laboratory of Beijing (Syndromes and Formulas), Beijing University of Chinese Medicine, Beijing, China; Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing,
[Ti] Título:The protective effect of the active components of ERPC on diabetic peripheral neuropathy in rats.
[So] Source:J Ethnopharmacol;202:162-171, 2017 Apr 18.
[Is] ISSN:1872-7573
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:ETHNOPHARMACOLOGICAL RELEVANCE: Euonymus alatus, Radix trichosanthis, Panax notoginseng and Coptis chinensis are popular plants used in traditional Chinese medicine to treat diabetes. AIM OF THE STUDY: The aim of the study is to investigate the therapeutic effect of the active components of Euonymus alatus, Radix trichosanthis, Panax notoginseng and Coptis chinensis (cERPC) on diabetic peripheral neuropathy in the rats and explore the underlying mechanism involved. METHODS: After diabetes was induced in rats for 20 weeks, cERPC or water was administered for 12 weeks. After a hot plate test, motor nerve conduction velocity and sciatic nerve blood flow were determined; the sciatic nerves were isolated for toluidine blue staining; and the fibre area, fibre diameter, axon area, axon diameter and myelin thickness were evaluated. The levels of the myelin basic protein, myelin protein zero, Oct6 and Krox20 were measured by western blot or immunofluorescence. RESULTS: cERPC was efficient in reducing the response latency, increasing motor nerve conduction velocity, enhancing sciatic nerve blood flow and ameliorating the pathological changes in diabetic rats. cERPC also had a role in increasing the levels of myelin basic protein and myelin protein zero and improving the expression of Oct6 and Krox20 in sciatic nerves of diabetic rats. CONCLUSIONS: cERPC ameliorates diabetic peripheral neuropathy by attenuating electrophysiological, circulatory and morphological alterations, which is mediated by the Oct6-Krox20 pathway.
[Mh] Termos MeSH primário: Neuropatias Diabéticas/prevenção & controle
Medicamentos de Ervas Chinesas/uso terapêutico
Substâncias Protetoras/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Axônios/patologia
Axônios/ultraestrutura
Diabetes Mellitus Experimental/tratamento farmacológico
Neuropatias Diabéticas/patologia
Masculino
Neurônios Motores/efeitos dos fármacos
Proteínas da Mielina/metabolismo
Bainha de Mielina/efeitos dos fármacos
Bainha de Mielina/patologia
Bainha de Mielina/ultraestrutura
Condução Nervosa/efeitos dos fármacos
Medição da Dor/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Fluxo Sanguíneo Regional/efeitos dos fármacos
Nervo Isquiático/irrigação sanguínea
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Myelin Proteins); 0 (Protective Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE


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[PMID]:28302146
[Au] Autor:Singh S; Dallenga T; Winkler A; Roemer S; Maruschak B; Siebert H; Brück W; Stadelmann C
[Ad] Endereço:Institute of Neuropathology, University Medical Center, Göttingen, Germany.
[Ti] Título:Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis.
[So] Source:J Neuroinflammation;14(1):57, 2017 Mar 17.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. METHODS: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (Wld ) mutant mice. RESULTS: The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in Wld mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. CONCLUSIONS: Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss.
[Mh] Termos MeSH primário: Axônios/patologia
Encéfalo/metabolismo
Pessoas com Deficiência
Esclerose Múltipla/complicações
Esclerose Múltipla/patologia
Degeneração Walleriana/etiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Precursor de Proteína beta-Amiloide/metabolismo
Animais
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/patologia
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Meia-Idade
Proteínas da Mielina/metabolismo
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Ciática/patologia
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Myelin Proteins); 0 (Nerve Tissue Proteins); 0 (Wld protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-017-0831-8


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[PMID]:28284349
[Au] Autor:Moriguchi K; Miyamoto K; Kusunoki S
[Ad] Endereço:Division of Neurology, Department of Internal Medicine 3, National Defense Medical College, Tokorozawa, Japan; Department of Internal Medicine, Japan Self Defense Forces Hanshin Hospital, Kawanishi, Japan.
[Ti] Título:4-Aminopyridine ameliorates experimental autoimmune neuritis in Lewis rats.
[So] Source:J Neuroimmunol;305:72-74, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We investigated the effect of 4-aminopyridine (4-AP) on experimental autoimmune neuritis (EAN) using a 4-AP-treated group in which 4-AP was administered in the diet, and a control group (n=10 per group). Electrophysiological and pathological assessment was performed in the sciatic nerve. The EAN clinical scores were significantly lower in the 4-AP-treated group than in the control group (p<0.05). The motor conductance velocity two weeks post-immunization was significantly higher in the 4-AP-treated group (p<0.05). Finally, 4-AP did not lead to pathological changes. Thus, 4-AP might be a potential therapeutic agent in demyelinating neuropathy.
[Mh] Termos MeSH primário: 4-Aminopiridina/uso terapêutico
Neurite Autoimune Experimental/tratamento farmacológico
Bloqueadores dos Canais de Potássio/uso terapêutico
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Animais
Modelos Animais de Doenças
Eletromiografia
Potencial Evocado Motor/efeitos dos fármacos
Potencial Evocado Motor/fisiologia
Adjuvante de Freund/toxicidade
Masculino
Proteínas da Mielina/toxicidade
Condução Nervosa/efeitos dos fármacos
Neurite Autoimune Experimental/induzido quimicamente
Neurite Autoimune Experimental/imunologia
Bloqueadores dos Canais de Potássio/farmacologia
Ratos
Ratos Endogâmicos Lew
Estatísticas não Paramétricas
Vacinação/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myelin Proteins); 0 (P2 peptide); 0 (Potassium Channel Blockers); 9007-81-2 (Freund's Adjuvant); BH3B64OKL9 (4-Aminopyridine)
[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


  10 / 5204 MEDLINE  
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[PMID]:28251916
[Au] Autor:Bansagi B; Griffin H; Whittaker RG; Antoniadi T; Evangelista T; Miller J; Greenslade M; Forester N; Duff J; Bradshaw A; Kleinle S; Boczonadi V; Steele H; Ramesh V; Franko E; Pyle A; Lochmüller H; Chinnery PF; Horvath R
[Ad] Endereço:From the MRC Centre for Neuromuscular Diseases and John Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine (B.B., H.G., T.E., J.D., A.B., V.B., H.S., E.F., A.P., H.L., P.F.C., R.H.), and Institute of Neuroscience (R.G.W., J.M.), Newcastle University, Newcastle upon Tyne; Bristo
[Ti] Título:Genetic heterogeneity of motor neuropathies.
[So] Source:Neurology;88(13):1226-1234, 2017 Mar 28.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To study the prevalence, molecular cause, and clinical presentation of hereditary motor neuropathies in a large cohort of patients from the North of England. METHODS: Detailed neurologic and electrophysiologic assessments and next-generation panel testing or whole exome sequencing were performed in 105 patients with clinical symptoms of distal hereditary motor neuropathy (dHMN, 64 patients), axonal motor neuropathy (motor Charcot-Marie-Tooth disease [CMT2], 16 patients), or complex neurologic disease predominantly affecting the motor nerves (hereditary motor neuropathy plus, 25 patients). RESULTS: The prevalence of dHMN is 2.14 affected individuals per 100,000 inhabitants (95% confidence interval 1.62-2.66) in the North of England. Causative mutations were identified in 26 out of 73 index patients (35.6%). The diagnostic rate in the dHMN subgroup was 32.5%, which is higher than previously reported (20%). We detected a significant defect of neuromuscular transmission in 7 cases and identified potentially causative mutations in 4 patients with multifocal demyelinating motor neuropathy. CONCLUSIONS: Many of the genes were shared between dHMN and motor CMT2, indicating identical disease mechanisms; therefore, we suggest changing the classification and including dHMN also as a subcategory of Charcot-Marie-Tooth disease. Abnormal neuromuscular transmission in some genetic forms provides a treatable target to develop therapies.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/epidemiologia
Heterogeneidade Genética
Neuropatia Hereditária Motora e Sensorial/epidemiologia
Neuropatia Hereditária Motora e Sensorial/genética
Mutação/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Análise de Variância
Doença de Charcot-Marie-Tooth/genética
Doença de Charcot-Marie-Tooth/fisiopatologia
Estudos de Coortes
Conexinas/genética
Análise Mutacional de DNA
Eletromiografia
Inglaterra/epidemiologia
Saúde da Família
Feminino
GTP Fosfo-Hidrolases/genética
Neuropatia Hereditária Motora e Sensorial/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Proteínas Mitocondriais/genética
Proteínas da Mielina/genética
Condução Nervosa/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (Mitochondrial Proteins); 0 (Myelin Proteins); 0 (PMP22 protein, human); 0 (connexin 32); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (MFN2 protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003772



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