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[PMID]:28207840
[Au] Autor:Zange J; Schopen K; Albracht K; Gerlach DA; Frings-Meuthen P; Maffiuletti NA; Bloch W; Rittweger J
[Ad] Endereço:Division of Space Physiology, Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany.
[Ti] Título:Using the Hephaistos orthotic device to study countermeasure effectiveness of neuromuscular electrical stimulation and dietary lupin protein supplementation, a randomised controlled trial.
[So] Source:PLoS One;12(2):e0171562, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The present study investigated whether neuromuscular electrical stimulation for 20 min twice a day with an electrode placed over the soleus muscle and nutritional supplementation with 19 g of protein rich lupin seeds can reduce the loss in volume and strength of the human calf musculature during long term unloading by wearing an orthotic unloading device. METHODS: Thirteen healthy male subjects (age of 26.4 ± 3.7 years) wore a Hephaistos orthosis one leg for 60 days during all habitual activities. The leg side was randomly chosen for every subject. Six subjects only wore the orthosis as control group, and 7 subjects additionally received the countermeasure consisting of neuromuscular electrical stimulation of the soleus and lateral gastrocnemius muscles and lupin protein supplementation. Twenty-eight days before and on the penultimate day of the intervention cross-sectional images of the calf muscles were taken by magnetic resonance imaging (controls n = 5), and maximum voluntary torque (controls n = 6) of foot plantar flexion was estimated under isometric (extended knee, 90° knee flexion) and isokinetic conditions (extended knee), respectively. RESULTS: After 58 days of wearing the orthosis the percentage loss of volume in the entire triceps surae muscle of the control subjects (-11.9 ± 4.4%, mean ± standard deviation) was reduced by the countermeasure (-3.5 ± 7.2%, p = 0.032). Wearing the orthosis generally reduced plantar flexion torques values, however, only when testing isometric contraction at 90° knee ankle the countermeasure effected a significantly lower percentage decrease of torque (-9.7 ± 7.2%, mean ± SD) in comparison with controls (-22.3 ± 11.2%, p = 0.032). CONCLUSION: Unloading of calf musculature by an orthotic device resulted in the expected loss of muscle volume and maximum of plantar flexion torque. Neuromuscular electrical muscle stimulation and lupin protein supplementation could significantly reduce the process of atrophy. TRIAL REGISTRATION: ClinicalTrials.gov, identifier NCT02698878.
[Mh] Termos MeSH primário: Proteínas na Dieta/uso terapêutico
Suplementos Nutricionais
Terapia por Estimulação Elétrica/métodos
Lupinus/química
Doenças da Junção Neuromuscular/terapia
Aparelhos Ortopédicos/utilização
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Estudos Transversais
Eletromiografia
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Dietary Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171562


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[PMID]:28082429
[Au] Autor:Greising SM; Vasdev AK; Zhan WZ; Sieck GC; Mantilla CB
[Ad] Endereço:Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
[Ti] Título:Chronic TrkB agonist treatment in old age does not mitigate diaphragm neuromuscular dysfunction.
[So] Source:Physiol Rep;5(1), 2017 Jan.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previously, we found that brain-derived neurotrophic factor (BDNF) signaling through the high-affinity tropomyosin-related kinase receptor subtype B (TrkB) enhances neuromuscular transmission in the diaphragm muscle. However, there is an age-related loss of this effect of BDNF/TrkB signaling that may contribute to diaphragm muscle sarcopenia (atrophy and force loss). We hypothesized that chronic treatment with 7,8-dihydroxyflavone (7,8-DHF), a small molecule BDNF analog and TrkB agonist, will mitigate age-related diaphragm neuromuscular transmission failure and sarcopenia in old mice. Adult male TrkB mice (n = 32) were randomized to the following 6-month treatment groups: vehicle-control, 7,8-DHF, and 7,8-DHF and 1NMPP1 (an inhibitor of TrkB kinase activity in TrkB mice) cotreatment, beginning at 18 months of age. At 24 months of age, diaphragm neuromuscular transmission failure, muscle-specific force, and fiber cross-sectional areas were compared across treatment groups. The results did not support our hypothesis in that chronic 7,8-DHF treatment did not improve diaphragm neuromuscular transmission or mitigate diaphragm muscle sarcopenia. Taken together, these results do not exclude a role for BDNF/TrkB signaling in aging-related changes in the diaphragm muscle, but they do not support the use of 7,8-DHF as a therapeutic agent to mitigate age-related neuromuscular dysfunction.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/metabolismo
Diafragma/inervação
Flavonas/farmacologia
Doenças da Junção Neuromuscular/fisiopatologia
Receptor trkB/antagonistas & inibidores
[Mh] Termos MeSH secundário: Envelhecimento/metabolismo
Envelhecimento/fisiologia
Animais
Fator Neurotrófico Derivado do Encéfalo/farmacologia
Diafragma/efeitos dos fármacos
Diafragma/fisiopatologia
Flavonas/administração & dosagem
Flavonas/metabolismo
Masculino
Camundongos
Doenças da Junção Neuromuscular/tratamento farmacológico
Pirazóis/administração & dosagem
Pirazóis/farmacologia
Pirimidinas/administração & dosagem
Pirimidinas/farmacologia
Receptor trkB/metabolismo
Receptor trkB/farmacologia
Sarcopenia/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-tert-butyl-3-naphthalen-1-ylmethyl-1H-pyrazolo(3,4-d)pyrimidin-4-ylemine); 0 (6,7-dihydroxyflavone); 0 (Brain-Derived Neurotrophic Factor); 0 (Flavones); 0 (Pyrazoles); 0 (Pyrimidines); EC 2.7.10.1 (Receptor, trkB)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE


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[PMID]:28006862
[Au] Autor:Krzesniak-Swinarska M; Caress JB; Cartwright MS
[Ad] Endereço:Department of Neurology, Wake Forest School of Medicine, Main Floor Reynolds Tower, Winston-Salem, North Carolina, 27157, USA.
[Ti] Título:Neuromuscular ultrasound for evaluation of scapular winging.
[So] Source:Muscle Nerve;56(1):7-14, 2017 Jul.
[Is] ISSN:1097-4598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Clinicians who treat nerve and muscle disorders may be asked to evaluate patients who have unilateral or bilateral scapular winging. Traditionally, this evaluation has relied upon a thorough history, physical examination, and electrodiagnostic testing to localize the cause of winging and detect the underlying neuromuscular pathology. Neuromuscular ultrasound has emerged as a non-invasive technique that can be used for structural evaluation of nerve and muscle abnormalities. METHODS: Previous studies of imaging in scapular winging and experiences from our diagnostic laboratory are reviewed. RESULTS: Four standard and 4 ancillary ultrasound views are described for evaluation of scapular winging. CONCLUSION: Ultrasound is a non-invasive, painless, and radiation-free technology that can be used to evaluate scapular winging. Muscle Nerve 56: 7-14, 2017.
[Mh] Termos MeSH primário: Músculo Esquelético/diagnóstico por imagem
Doenças da Junção Neuromuscular/diagnóstico por imagem
Escápula/diagnóstico por imagem
Ultrassonografia
[Mh] Termos MeSH secundário: Seres Humanos
Músculo Esquelético/inervação
Escápula/inervação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:161223
[St] Status:MEDLINE
[do] DOI:10.1002/mus.25533


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[PMID]:27382038
[Au] Autor:Hughes DC; Marcotte GR; Marshall AG; West DWD; Baehr LM; Wallace MA; Saleh PM; Bodine SC; Baar K
[Ad] Endereço:Department of Neurobiology, Physiology and Behavior and.
[Ti] Título:Age-related Differences in Dystrophin: Impact on Force Transfer Proteins, Membrane Integrity, and Neuromuscular Junction Stability.
[So] Source:J Gerontol A Biol Sci Med Sci;72(5):640-648, 2017 May 01.
[Is] ISSN:1758-535X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The loss of muscle strength with age has been studied from the perspective of a decline in muscle mass and neuromuscular junction (NMJ) stability. A third potential factor is force transmission. The purpose of this study was to determine the changes in the force transfer apparatus within aging muscle and the impact on membrane integrity and NMJ stability. We measured an age-related loss of dystrophin protein that was greatest in the flexor muscles. The loss of dystrophin protein occurred despite a twofold increase in dystrophin mRNA. Importantly, this disparity could be explained by the four- to fivefold upregulation of the dystromir miR-31. To compensate for the loss of dystrophin protein, aged muscle contained increased α-sarcoglycan, syntrophin, sarcospan, laminin, ß1-integrin, desmuslin, and the Z-line proteins α-actinin and desmin. In spite of the adaptive increase in other force transfer proteins, over the 48 hours following lengthening contractions, the old muscles showed more signs of impaired membrane integrity (fourfold increase in immunoglobulin G-positive fibers and 70% greater dysferlin mRNA) and NMJ instability (14- to 96-fold increases in Runx1, AchRδ, and myogenin mRNA). Overall, these data suggest that age-dependent alterations in dystrophin leave the muscle membrane and NMJ more susceptible to contraction-induced damage even before changes in muscle mass are obvious.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Distrofina/metabolismo
Músculo Esquelético/metabolismo
Doenças da Junção Neuromuscular/metabolismo
Junção Neuromuscular/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Estimulação Elétrica
Imuno-Histoquímica
Contração Muscular
Proteínas Musculares/metabolismo
RNA/análise
Ratos
Ratos Endogâmicos F344
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dystrophin); 0 (Muscle Proteins); 63231-63-0 (RNA)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE
[do] DOI:10.1093/gerona/glw109


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[PMID]:27615030
[Au] Autor:Su X; Kang PB; Russell JA; Simmons Z
[Ad] Endereço:Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
[Ti] Título:Ethical issues in the evaluation of adults with suspected genetic neuromuscular disorders.
[So] Source:Muscle Nerve;54(6):997-1006, 2016 Dec.
[Is] ISSN:1097-4598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic testing is rapidly becoming an increasingly significant part of the diagnostic armamentarium of neuromuscular clinicians. Although technically easy to order, the results of such testing, whether positive or negative, have potentially enormous consequences for the individual tested and for family members. As a result, ethical considerations must be in the forefront of the physician's agenda when obtaining genetic testing. Informed consent is an important starting point for discussions between physicians and patients, but the counseling embedded in the informed consent process must be an ongoing part of subsequent interactions, including return of results and follow-up. Patient autonomy, including the right to know and right not-to-know results, must be respected. Considerations of capacity, physician beneficence and nonmaleficence, and privacy all play roles in the process. Muscle Nerve 54: 997-1006, 2016.
[Mh] Termos MeSH primário: Beneficência
Ética Médica
Doenças da Junção Neuromuscular/genética
[Mh] Termos MeSH secundário: Testes Genéticos
Seres Humanos
Consentimento Livre e Esclarecido
Doenças da Junção Neuromuscular/diagnóstico
[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:160913
[St] Status:MEDLINE
[do] DOI:10.1002/mus.25400


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[PMID]:27567739
[Au] Autor:Talbot JD; Barrett JN; Nonner D; Zhang Z; Wicomb K; Barrett EF
[Ad] Endereço:Department of Physiology and Biophysics, University of Miami Miller School of Medicine, P.O. Box 016430, Miami, FL 33101, USA.
[Ti] Título:Preservation of neuromuscular function in symptomatic SOD1-G93A mice by peripheral infusion of methylene blue.
[So] Source:Exp Neurol;285(Pt A):96-107, 2016 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In mutant superoxide dismutase 1 (SOD1) mouse models of familial amyotrophic lateral sclerosis (fALS) some of the earliest signs of morphological and functional damage occur in the motor nerve terminals that innervate fast limb muscles. This study tested whether localized peripheral application of a protective drug could effectively preserve neuromuscular junctions in late-stage disease. Methylene blue (MB), which has mitochondria-protective properties, was infused via an osmotic pump into the anterior muscle compartment of one hind limb of late pre- symptomatic SOD1-G93A mice for ≥3weeks. When mice reached end-stage disease, peak twitch and tetanic contractions evoked by stimulation of the muscle nerve were measured in two anterior compartment muscles (tibialis anterior [TA] and extensor digitorum longus [EDL], both predominantly fast muscles). With 400µM MB in the infusion reservoir, muscles on the MB-infused side exhibited on average a ~100% increase in nerve-evoked contractile force compared to muscles on the contralateral non-infused side (p<0.01 for both twitch and tetanus in EDL and TA). Pairwise comparisons of endplate innervation also revealed a beneficial effect of MB infusion, with an average of 65% of endplates innervated in infused EDL, compared to only 35% on the non-infused side (p<0.01). Results suggested that MB's protective effects required an extracellular [MB] of ~1µM, were initiated peripherally (no evidence of retrograde transport into the spinal cord), and involved MB's reduced form. Thus peripherally-initiated actions of MB can help preserve neuromuscular structure and function in SOD1-G93A mice, even at late stages of disease.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/complicações
Inibidores Enzimáticos/administração & dosagem
Azul de Metileno/administração & dosagem
Doenças da Junção Neuromuscular/tratamento farmacológico
Doenças da Junção Neuromuscular/etiologia
Superóxido Dismutase/genética
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/tratamento farmacológico
Esclerose Amiotrófica Lateral/genética
Esclerose Amiotrófica Lateral/patologia
Animais
Bungarotoxinas/farmacocinética
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Sistemas de Liberação de Medicamentos
Inibidores Enzimáticos/uso terapêutico
Imunofluorescência
Seres Humanos
Azul de Metileno/uso terapêutico
Camundongos
Camundongos Transgênicos
Placa Motora/efeitos dos fármacos
Placa Motora/fisiologia
Contração Muscular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bungarotoxins); 0 (Enzyme Inhibitors); EC 1.15.1.1 (SOD1 G93A protein); EC 1.15.1.1 (Superoxide Dismutase); T42P99266K (Methylene Blue)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160829
[St] Status:MEDLINE


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[PMID]:27112691
[Au] Autor:Verschuuren J; Strijbos E; Vincent A
[Ad] Endereço:Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands. Electronic address: j.j.g.m.verschuuren@lumc.nl.
[Ti] Título:Neuromuscular junction disorders.
[So] Source:Handb Clin Neurol;133:447-66, 2016.
[Is] ISSN:0072-9752
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Diseases of the neuromuscular junction comprise a wide range of disorders. Antibodies, genetic mutations, specific drugs or toxins interfere with the number or function of one of the essential proteins that control signaling between the presynaptic nerve ending and the postsynaptic muscle membrane. Acquired autoimmune disorders of the neuromuscular junction are the most common and are described here. In myasthenia gravis, antibodies to acetylcholine receptors or to proteins involved in receptor clustering, particularly muscle-specific kinase, cause direct loss of acetylcholine receptors or interfere with the agrin-induced acetylcholine receptor clustering necessary for efficient neurotransmission. In the Lambert-Eaton myasthenic syndrome (LEMS), loss of the presynaptic voltage-gated calcium channels results in reduced release of the acetylcholine transmitter. The conditions are generally recognizable clinically and the diagnosis confirmed by serologic testing and electromyography. Screening for thymomas in myasthenia or small cell cancer in LEMS is important. Fortunately, a wide range of symptomatic treatments, immunosuppressive drugs, or other immunomodulating therapies is available. Future research is directed to understanding the pathogenesis, discovering new antigens, and trying to develop disease-specific treatments.
[Mh] Termos MeSH primário: Doenças da Junção Neuromuscular
Junção Neuromuscular/patologia
[Mh] Termos MeSH secundário: Autoanticorpos/metabolismo
Eletromiografia
Seres Humanos
Junção Neuromuscular/fisiopatologia
Doenças da Junção Neuromuscular/diagnóstico
Doenças da Junção Neuromuscular/imunologia
Doenças da Junção Neuromuscular/fisiopatologia
Receptores Colinérgicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170209
[Lr] Data última revisão:
170209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160427
[St] Status:MEDLINE


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[PMID]:26921370
[Au] Autor:Scurry AN; Heredia DJ; Feng CY; Gephart GB; Hennig GW; Gould TW
[Ad] Endereço:From the Departments of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.
[Ti] Título:Structural and Functional Abnormalities of the Neuromuscular Junction in the Trembler-J Homozygote Mouse Model of Congenital Hypomyelinating Neuropathy.
[So] Source:J Neuropathol Exp Neurol;75(4):334-46, 2016 Apr.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mutations in peripheral myelin protein 22 (PMP22) result in the most common form of Charcot-Marie-Tooth (CMT) disease, CMT1A. This hereditary peripheral neuropathy is characterized by dysmyelination of peripheral nerves, reduced nerve conduction velocity, and muscle weakness. APMP22 point mutation in L16P (leucine 16 to proline) underlies a form of human CMT1A as well as the Trembler-J mouse model of CMT1A. Homozygote Trembler-J mice (Tr(J)) die early postnatally, fail to make peripheral myelin, and, therefore, are more similar to patients with congenital hypomyelinating neuropathy than those with CMT1A. Because recent studies of inherited neuropathies in humans and mice have demonstrated that dysfunction and degeneration of neuromuscular synapses or junctions (NMJs) often precede impairments in axonal conduction, we examined the structure and function of NMJs in Tr(J)mice. Although synapses appeared to be normally innervated even in end-stage Tr(J)mice, the growth and maturation of the NMJs were altered. In addition, the amplitudes of nerve-evoked muscle endplate potentials were reduced and there was transmission failure during sustained nerve stimulation. These results suggest that the severe congenital hypomyelinating neuropathy that characterizes Tr(J)mice results in structural and functional deficits of the developing NMJ.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/genética
Doença de Charcot-Marie-Tooth/patologia
Modelos Animais de Doenças
Proteínas da Mielina/genética
Doenças da Junção Neuromuscular/etiologia
Doenças da Junção Neuromuscular/patologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Diafragma/patologia
Diafragma/ultraestrutura
Estimulação Elétrica
Potenciais Evocados/genética
Homozigoto
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Transgênicos
Microscopia Eletrônica
Condução Nervosa/genética
Junção Neuromuscular/patologia
Junção Neuromuscular/ultraestrutura
Doenças da Junção Neuromuscular/genética
Mutação Puntual/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Myelin Proteins); 0 (PMP22 protein, human)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160228
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlw004


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[PMID]:26870889
[Au] Autor:Rudolf R; Deschenes MR; Sandri M
[Ad] Endereço:aInterdisciplinary Center for Neuroscience, University of Heidelberg, Heidelberg bInstitute of Molecular and Cell Biology, Mannheim University of Applied Science, Mannheim cInstitute of Toxicology and Genetics, Karlsruhe Institute of Technology, Karlsruhe, Germany dDepartment of Kinesiology and Health Sciences, The College of William and Mary, Williamsburg, Virginia, USA eDepartment of Biomedical Science, University of Padua fVenetian Institute of Molecular Medicine (VIMM), Padua, Italy.
[Ti] Título:Neuromuscular junction degeneration in muscle wasting.
[So] Source:Curr Opin Clin Nutr Metab Care;19(3):177-81, 2016 May.
[Is] ISSN:1473-6519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Denervation is a hallmark of age-related and other types of muscle wasting. This review focuses on recent insights and current viewpoints regarding the mechanisms and clinical relevance of maintaining the neuromuscular junction to counteract muscle wasting resulting from aging or neural disease/damage. RECENT FINDINGS: Activity-dependent regulation of autophagy, the agrin-muscle specific kinase-Lrp4 signaling axis, and sympathetic modulation are principal mechanisms involved in stabilizing the neuromuscular junction. These findings are derived from several animal models and were largely confirmed by human gene expression analysis as well as insights from rare neuromuscular diseases such as amyotrophic lateral sclerosis and congenital myasthenic syndromes. Based on these insights, agrin-derived fragments are currently being evaluated as biomarkers for age-related muscle wasting. Tuning of autophagy, of the agrin pathway, and of sympathetic input are being studied as clinical treatment of muscle wasting disorders. SUMMARY: Basic research has revealed that maintenance of neuromuscular junctions and a few signaling pathways are important in the context of age-dependent and other forms of muscle wasting. These findings have recently started to enter clinical practice, but further research needs to substantiate and refine our knowledge.
[Mh] Termos MeSH primário: Modelos Biológicos
Atrofia Muscular/etiologia
Degeneração Neural/etiologia
Doenças da Junção Neuromuscular/etiologia
Junção Neuromuscular/fisiopatologia
Síndrome de Emaciação/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Autofagia
Regulação da Expressão Gênica
Seres Humanos
Proteínas Musculares/agonistas
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Junção Neuromuscular/metabolismo
Junção Neuromuscular/patologia
Síndrome de Emaciação/metabolismo
Síndrome de Emaciação/patologia
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Muscle Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160213
[St] Status:MEDLINE
[do] DOI:10.1097/MCO.0000000000000267


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[PMID]:26831261
[Au] Autor:Ashraf GM; Ali A; Tabrez S; Zaidi SK; Shakil S; Alam MZ; Rehan M; Aliev G
[Ti] Título:Linkage of Stress with Neuromuscular Disorders.
[So] Source:CNS Neurol Disord Drug Targets;15(3):321-8, 2016.
[Is] ISSN:1996-3181
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:Aging is associated with a progressive loss of muscle strength and mass, and a decline in neurophysiologic functions, which are characteristic features of neuromuscular disorders (NMDs). Understanding aging induced neuromuscular junction (NMJ) dysfunction is very crucial to understand the mechanism underlying NMDs. Morphological and physiological changes result in remodelling of the motor unit and a decline in the number of motor neuron muscle fibres. These alterations lead to excitation-contraction uncoupling and a loss of communication between the neuromuscular system, causing a decline in skeletal muscle strength and muscle mass. Understanding the molecular basis of NMJ dysfunction is essential in search for new treatment options. Besides structural and molecular studies, search for animal models to establish connection between brain and muscle is needed. Among various factors it has been observed that stress is one of the leading causes of NMDs. In the present review, we aim to explore various factors linking stress and NMDs neuromuscular disorders which gets aggravated by aging, with a special emphasis on mitochondrial connection. This in turn will help us gain new insights in the treatment of NMDs by aiding in improved symptoms, increased mobility and prolonged life.
[Mh] Termos MeSH primário: Força Muscular/fisiologia
Doenças da Junção Neuromuscular/fisiopatologia
Estresse Oxidativo/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
Doenças da Junção Neuromuscular/patologia
Estresse Mecânico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE



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