Base de dados : MEDLINE
Pesquisa : C10.574.562 [Categoria DeCS]
Referências encontradas : 3905 [refinar]
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[PMID]:29363539
[Au] Autor:Pirmohamed M
[Ad] Endereço:Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
[Ti] Título:Nucleic acid based therapies: developing frontier for precision medicine.
[So] Source:BMJ;360:k223, 2018 01 23.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Terapia Genética/utilização
Terapia de Alvo Molecular/utilização
Ácidos Nucleicos/uso terapêutico
Medicina de Precisão/métodos
[Mh] Termos MeSH secundário: Adenoviridae/genética
Aminofenóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Regulador de Condutância Transmembrana em Fibrose Cística/efeitos dos fármacos
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Terapia Genética/economia
Genômica
Hemofilia A/classificação
Hemofilia A/tratamento farmacológico
Hemofilia A/genética
Seres Humanos
Doença dos Neurônios Motores/tratamento farmacológico
Doença dos Neurônios Motores/genética
Mutação
Oligonucleotídeos Antissenso/economia
Oligonucleotídeos Antissenso/uso terapêutico
Quinolonas/uso terapêutico
Reino Unido/epidemiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Aminophenols); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Nucleic Acids); 0 (Oligonucleotides, Antisense); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k223


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[PMID]:29367349
[Au] Autor:Ezekiel S
[Ti] Título:"Where there is life, there is hope".
[So] Source:BMJ;360:j5920, 2018 01 24.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Esperança
Doença dos Neurônios Motores/psicologia
[Mh] Termos MeSH secundário: Adulto
Atitude Frente à Saúde
Feminino
Cuidados Paliativos na Terminalidade da Vida
Seres Humanos
Doença dos Neurônios Motores/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; PERSONAL NARRATIVES
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5920


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[PMID]:28745069
[Au] Autor:de Vries BS; Rustemeijer LMM; van der Kooi AJ; Raaphorst J; Schröder CD; Nijboer TCW; Hendrikse J; Veldink JH; van den Berg LH; van Es MA
[Ad] Endereço:a Department of Neurology , Brain Center Rudolf Magnus, University Medical Center Utrecht , Utrecht , The Netherlands.
[Ti] Título:A case series of PLS patients with frontotemporal dementia and overview of the literature.
[So] Source:Amyotroph Lateral Scler Frontotemporal Degener;18(7-8):534-548, 2017 Nov.
[Is] ISSN:2167-9223
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Primary lateral sclerosis (PLS) is a rare form of motor neuron disease characterised by UMN degeneration leading to slowly progressive spasticity. Whether it is a separate disease or a subtype of ALS has been debated. In ALS comorbid frontotemporal dementia (FTD) is frequently seen (±15%). However, cognitive and behavioural changes are generally not considered to be a part of PLS. METHODS: To report the clinical findings and frequency of PLS patients that developed FTD in a referral-based cohort and provide an overview of the literature. RESULTS: In our cohort six out of 181 (3.3%) PLS patients developed FTD. In the literature a few cases of PLS with FTD have been reported and only a limited number of small studies have investigated cognition in PLS. However, when these studies are summarised a pattern emerges with FTD diagnoses in ±2% and frontotemporal impairment in 22% of patients. CONCLUSIONS: These findings suggest that PLS is part of the FTD-MND continuum and would favour viewing it as a subtype of ALS. It is, however, not a restricted (isolated UMN involvement) phenotype.
[Mh] Termos MeSH primário: Demência Frontotemporal/diagnóstico
Doença dos Neurônios Motores/diagnóstico
Avaliação de Sintomas/métodos
[Mh] Termos MeSH secundário: Idoso
Diagnóstico Diferencial
Feminino
Demência Frontotemporal/classificação
Demência Frontotemporal/complicações
Seres Humanos
Masculino
Meia-Idade
Doença dos Neurônios Motores/classificação
Doença dos Neurônios Motores/complicações
Fatores de Risco
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1080/21678421.2017.1354996


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[PMID]:28859337
[Au] Autor:Takeda T; Seilhean D; Le Ber I; Millecamps S; Sazdovitch V; Kitagawa K; Uchihara T; Duyckaerts C
[Ad] Endereço:Service de Neuropathologie, Laboratoire Raymond Escourolle, AP-HP, Hôpitaux Universitaires La Pitié Salpêtrière-Charles Foix, Hôpital de la Pitié-Salpêtrière, Paris, France; Institut du Cerveau et de la Moelle Épinière (ICM), INSERM U1127, CNRS UMR 7225, Sorbonne Universités, Université Pierre et Ma
[Ti] Título:Amygdala TDP-43 Pathology in Frontotemporal Lobar Degeneration and Motor Neuron Disease.
[So] Source:J Neuropathol Exp Neurol;76(9):800-812, 2017 Sep 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:TDP-43-positive inclusions are present in the amygdala in frontotemporal lobar degeneration (FTLD) and motor neuron disease (MND) including amyotrophic lateral sclerosis. Behavioral abnormalities, one of the chief symptoms of FTLD, could be, at least partly, related to amygdala pathology. We examined TDP-43 inclusions in the amygdala of patients with sporadic FTLD/MND (sFTLD/MND), FTLD/MND with mutation of the C9ORF72 (FTLD/MND-C9) and FTLD with mutation of the progranulin (FTLD-GRN). TDP-43 inclusions were common in each one of these subtypes, which can otherwise be distinguished on topographical and genetic grounds. Conventional and immunological stainings were performed and we quantified the numerical density of inclusions on a regional basis. TDP-43 inclusions in amygdala could be seen in 10 out of 26 sFTLD/MND cases, 5 out of 9 FTLD/MND-C9 cases, and all 4 FTLD-GRN cases. Their numerical density was lower in FTLD/MND-C9 than in sFTLD/MND and FTLD-GRN. TDP-43 inclusions were more numerous in the ventral region of the basolateral nucleus group in all subtypes. This contrast was apparent in sporadic and C9-mutated FTLD/MND, while it was less evident in FTLD-GRN. Such differences in subregional involvement of amygdala may be related to the region-specific neuronal connections that are differentially affected in FTLD/MND and FTLD-GRN.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/metabolismo
Proteínas de Ligação a DNA/metabolismo
Degeneração Lobar Frontotemporal/patologia
Doença dos Neurônios Motores/patologia
[Mh] Termos MeSH secundário: Idoso
Proteína C9orf72
Feminino
Regulação da Expressão Gênica/genética
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Masculino
Meia-Idade
Mutação/genética
Proteínas/metabolismo
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (C9orf72 Protein); 0 (C9orf72 protein, human); 0 (DNA-Binding Proteins); 0 (GRN protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Proteins); 0 (TDP-43 protein, human); 0 (tau Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx063


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[PMID]:28837908
[Au] Autor:Garg N; Howells J; Yiannikas C; Vucic S; Krishnan AV; Spies J; Bostock H; Mathey EK; Pollard JD; Park SB; Kiernan MC
[Ad] Endereço:Brain and Mind Centre, Sydney Medical School, The University of Sydney, 94 Mallett St, Camperdown, NSW 2050, Australia; Department of Neurology, Royal Prince Alfred Hospital, The University of Sydney, NSW, Australia. Electronic address: nidhi.garg@sydney.edu.au.
[Ti] Título:Motor unit remodelling in multifocal motor neuropathy: The importance of axonal loss.
[So] Source:Clin Neurophysiol;128(10):2022-2028, 2017 Oct.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To estimate the degree of axonal loss in patients diagnosed with multifocal motor neuropathy (MMN) using a novel assessment of motor unit numbers and size. METHODS: Automated motor unit number estimation using a compound muscle action potential (CMAP) scan was undertaken in median nerves with conduction block. Results were compared with 30 age-matched healthy controls. RESULTS: Compared with healthy controls, MMN patients had fewer motor units (MMN: 33±11vs HC: 93±36 [mean±SD]; p<0.0001) and larger 'size of the largest unit' (MMN: 1.2±0.5mVvs HC: 0.4±0.1mV; p<0.0001), despite having normal distal CMAP amplitudes (MMN: 7.6±1.8mVvs HC: 8.7±2.5mV; p=0.24). CONCLUSIONS: MMN is associated with marked axonal loss which may be masked by striking re-innervation resulting in preservation of distal CMAP amplitudes. SIGNIFICANCE: Assessment of motor unit properties should be incorporated into assessment of disease progression in MMN, given that nerve conduction studies are insensitive to motor unit remodelling.
[Mh] Termos MeSH primário: Axônios/fisiologia
Doença dos Neurônios Motores/fisiopatologia
Degeneração Neural/fisiopatologia
Polineuropatias/fisiopatologia
Recrutamento Neurofisiológico/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Adulto
Idoso
Estudos de Coortes
Feminino
Seres Humanos
Masculino
Meia-Idade
Doença dos Neurônios Motores/diagnóstico
Degeneração Neural/diagnóstico
Condução Nervosa/fisiologia
Polineuropatias/diagnóstico
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE


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[PMID]:28821644
[Au] Autor:Sugiyama K; Aida T; Nomura M; Takayanagi R; Zeilhofer HU; Tanaka K
[Ad] Endereço:Laboratory of Molecular Neuroscience, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.
[Ti] Título:Calpain-Dependent Degradation of Nucleoporins Contributes to Motor Neuron Death in a Mouse Model of Chronic Excitotoxicity.
[So] Source:J Neurosci;37(36):8830-8844, 2017 Sep 06.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glutamate-mediated excitotoxicity induces neuronal death by altering various intracellular signaling pathways and is implicated as a common pathogenic pathway in many neurodegenerative diseases. In the case of motor neuron disease, there is significant evidence to suggest that the overactivation of AMPA receptors due to deficiencies in the expression and function of glial glutamate transporters GLT1 and GLAST plays an important role in the mechanisms of neuronal death. However, a causal role for glial glutamate transporter dysfunction in motor neuron death remains unknown. Here, we developed a new animal model of excitotoxicity by conditionally deleting astroglial glutamate transporters GLT1 and GLAST in the spinal cords of mice (GLAST /GLT1-cKO). GLAST /GLT1-cKO mice (both sexes) exhibited nuclear irregularity and calpain-mediated degradation of nuclear pore complexes (NPCs), which are responsible for nucleocytoplasmic transport. These abnormalities were associated with progressive motor neuron loss, severe paralysis, and shortened lifespan. The nuclear export inhibitor KPT-350 slowed but did not prevent motor neuron death, whereas long-term treatment of the AMPA receptor antagonist perampanel and the calpain inhibitor SNJ-1945 had more persistent beneficial effects. Thus, NPC degradation contributes to AMPA receptor-mediated excitotoxic motor neuronal death, and preventing NPC degradation has robust protective effects. Normalization of NPC function could be a novel therapeutic strategy for neurodegenerative disorders in which AMPA receptor-mediated excitotoxicity is a contributory factor. Despite glial glutamate transporter dysfunction leading to excitotoxicity has been documented in many neurological diseases, it remains unclear whether its dysfunction is a primary cause or secondary outcome of neuronal death at disease state. Here we show the combined loss of glial glutamate transporters GLT1 and GLAST in spinal cord caused motor neuronal death and hindlimb paralysis. Further, our novel mutant exhibits the nuclear irregularities and calpain-mediated progressive nuclear pore complex degradation. Our study reveals that glial glutamate transporter dysfunction is sufficient to cause motor neuronal death .
[Mh] Termos MeSH primário: Apoptose
Calpaína/metabolismo
Modelos Animais de Doenças
Doença dos Neurônios Motores/metabolismo
Neurônios Motores/metabolismo
Complexo de Proteínas Formadoras de Poros Nucleares/metabolismo
Doenças da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Ativação Enzimática
Feminino
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Doença dos Neurônios Motores/patologia
Neurônios Motores/patologia
Doenças da Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Pore Complex Proteins); EC 3.4.22.- (Calpain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0730-17.2017


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[PMID]:28817497
[Au] Autor:Bassola B; Lusignani M
[Ad] Endereço:Maura Lusignani, RN MSC, is Associate Professor, University of Milan, Milan, Italy.
[Ti] Título:Self-care in People With Motor Neuron Disease: An Integrative Review.
[So] Source:J Neurosci Nurs;49(5):311-317, 2017 Oct.
[Is] ISSN:1945-2810
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Self-care is a crucial aspect in the management of chronic diseases. People with motor neuron disease (MND) live with a chronic degenerative condition in rapid evolution, which leads them to high dependencies. During their illness, they must apply several behaviors including adherence to ventilation and nutritional therapy. OBJECTIVE: The purpose of this review is to systematically explore the concept of self-care for people with MND. METHOD: An integrative review of the literature has been conducted. The electronic databases CINAHL, PubMed, and SCOPUS were searched. RESULTS: Fifteen articles met the inclusion criteria and were reviewed; 7 of them discuss decision-making process and adherence to ventilation and nutritional therapy. Five of them discuss strategies used by people with MND to optimize living with this illness. Four of them discuss care and monitoring behaviors performed and recommended to people with MND. No studies focused on self-care in people with MND was identified in the literature. CONCLUSIONS: The concept of self-care in people with MND is related to inventiveness, to adaptability, and to dependence. Further studies seem to be needed to understand the concept of self-care in this population.
[Mh] Termos MeSH primário: Doença Crônica
Tomada de Decisões
Doença dos Neurônios Motores/terapia
Autocuidado
[Mh] Termos MeSH secundário: Seres Humanos
Doença dos Neurônios Motores/dietoterapia
Doença dos Neurônios Motores/psicologia
Qualidade de Vida
Ventilação/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM; N
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1097/JNN.0000000000000303


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[PMID]:28686046
[Au] Autor:Vesey S
[Ad] Endereço:Clinical Lead Speech and language Therapist, Pennine Care NHS Foundation Trust Trafford General Hospital, Manchester.
[Ti] Título:The challenges of dysphagia in treating motor neurone disease.
[So] Source:Br J Community Nurs;22(Sup7):S17-S21, 2017 Jul 01.
[Is] ISSN:1462-4753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Motor neurone disease (MND) is a relatively rare degenerative disorder. Its impacts are manifested in progressive loss of motor function and often accompanied by wider non-motor changes. Swallowing and speech abilities are frequently severely impaired. Effective management of dysphagia (swallowing difficulty) symptoms and nutritional care requires a holistic multidisciplinary approach. Care must be patient focused, facilitate patient decision making, and support planning towards end of life care. This article discusses the challenges of providing effective nutritional care to people living with motor neurone disease who have dysphagia.
[Mh] Termos MeSH primário: Transtornos de Deglutição/enfermagem
Doença dos Neurônios Motores/enfermagem
[Mh] Termos MeSH secundário: Transtornos de Deglutição/etiologia
Transtornos de Deglutição/fisiopatologia
Disartria/etiologia
Disartria/fisiopatologia
Disfonia/etiologia
Disfonia/fisiopatologia
Nutrição Enteral
Gastrostomia
Seres Humanos
Doença dos Neurônios Motores/complicações
Doença dos Neurônios Motores/fisiopatologia
Qualidade de Vida
Assistência Terminal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.12968/bjcn.2017.22.Sup7.S17


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[PMID]:28446118
[Au] Autor:Dharmadasa T; Henderson RD; Talman PS; Macdonell RA; Mathers S; Schultz DW; Needham M; Zoing M; Vucic S; Kiernan MC
[Ad] Endereço:Brain and Mind Centre, University of Sydney, Sydney, NSW thanuja.dharmadasa@sydney.edu.au.
[Ti] Título:Motor neurone disease: progress and challenges.
[So] Source:Med J Aust;206(8):357-362, 2017 May 01.
[Is] ISSN:1326-5377
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Major progress has been made over the past decade in the understanding of motor neurone disease (MND), changing the landscape of this complex disease. Through identifying positive prognostic factors, new evidence-based standards of care have been established that improve patient survival, reduce burden of disease for patients and their carers, and enhance quality of life. These factors include early management of respiratory dysfunction with non-invasive ventilation, maintenance of weight and nutritional status, as well as instigation of a multidisciplinary team including neurologists, general practitioners and allied health professionals. Advances in technology have enhanced our understanding of the genetic architecture of MND considerably, with implications for patients, their families and clinicians. Recognition of extra-motor involvement, particularly cognitive dysfunction, has identified a spectrum of disease from MND through to frontotemporal dementia. Although riluzole remains the only disease-modifying medication available in clinical practice in Australia, several new therapies are undergoing clinical trials nationally and globally, representing a shift in treatment paradigms. Successful translation of this clinical research through growth in community funding, awareness and national MND research organisations has laid the foundation for closing the research-practice gap on this debilitating disease. In this review, we highlight these recent developments, which have transformed treatment, augmented novel therapeutic platforms, and established a nexus between research and the MND community. This era of change is of significant relevance to both specialists and general practitioners who remain integral to the care of patients with MND.
[Mh] Termos MeSH primário: Comunicação Interdisciplinar
Doença dos Neurônios Motores/terapia
Padrão de Cuidado
[Mh] Termos MeSH secundário: Austrália
Prática Clínica Baseada em Evidências
Testes Genéticos
Terapia Genética
Seres Humanos
Neuroproteção
Ventilação não Invasiva
Apoio Nutricional
Aceitação pelo Paciente de Cuidados de Saúde
Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
Transplante de Células-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:28362802
[Au] Autor:Kline RA; Kaifer KA; Osman EY; Carella F; Tiberi A; Ross J; Pennetta G; Lorson CL; Murray LM
[Ad] Endereço:Centre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
[Ti] Título:Comparison of independent screens on differentially vulnerable motor neurons reveals alpha-synuclein as a common modifier in motor neuron diseases.
[So] Source:PLoS Genet;13(3):e1006680, 2017 Mar.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The term "motor neuron disease" encompasses a spectrum of disorders in which motor neurons are the primary pathological target. However, in both patients and animal models of these diseases, not all motor neurons are equally vulnerable, in that while some motor neurons are lost very early in disease, others remain comparatively intact, even at late stages. This creates a valuable system to investigate the factors that regulate motor neuron vulnerability. In this study, we aim to use this experimental paradigm to identify potential transcriptional modifiers. We have compared the transcriptome of motor neurons from healthy wild-type mice, which are differentially vulnerable in the childhood motor neuron disease Spinal Muscular Atrophy (SMA), and have identified 910 transcriptional changes. We have compared this data set with published microarray data sets on other differentially vulnerable motor neurons. These neurons were differentially vulnerable in the adult onset motor neuron disease Amyotrophic Lateral Sclerosis (ALS), but the screen was performed on the equivalent population of neurons from neurologically normal human, rat and mouse. This cross species comparison has generated a refined list of differentially expressed genes, including CELF5, Col5a2, PGEMN1, SNCA, Stmn1 and HOXa5, alongside a further enrichment for synaptic and axonal transcripts. As an in vivo validation, we demonstrate that the manipulation of a significant number of these transcripts can modify the neurodegenerative phenotype observed in a Drosophila line carrying an ALS causing mutation. Finally, we demonstrate that vector-mediated expression of alpha-synuclein (SNCA), a transcript decreased in selectively vulnerable motor neurons in all four screens, can extend life span, increase weight and decrease neuromuscular junction pathology in a mouse model of SMA. In summary, we have combined multiple data sets to identify transcripts, which are strong candidates for being phenotypic modifiers, and demonstrated SNCA is a modifier of pathology in motor neuron disease.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Doença dos Neurônios Motores/genética
Neurônios Motores/metabolismo
alfa-Sinucleína/genética
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/patologia
Animais
Axônios/metabolismo
Axônios/patologia
Modelos Animais de Doenças
Drosophila melanogaster/genética
Regulação da Expressão Gênica/genética
Seres Humanos
Camundongos
Doença dos Neurônios Motores/patologia
Neurônios Motores/patologia
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Junção Neuromuscular/genética
Junção Neuromuscular/patologia
Fenótipo
Ratos
Transcriptoma/genética
alfa-Sinucleína/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Snca protein, mouse); 0 (alpha-Synuclein)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006680



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde