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  1 / 1867 MEDLINE  
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[PMID]:29287782
[Au] Autor:Liaquat L; Batool Z; Sadir S; Rafiq S; Shahzad S; Perveen T; Haider S
[Ad] Endereço:Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi 75270, Pakistan.
[Ti] Título:Naringenin-induced enhanced antioxidant defence system meliorates cholinergic neurotransmission and consolidates memory in male rats.
[So] Source:Life Sci;194:213-223, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Free radical mediated neurotoxicity is a leading cause of neurodegenerative disorders. Neurodegeneration due to oxidative stress can produce cognitive dysfunctions. Flavonoids and curcuminoids are naturally occurring polyphenolic compounds that display a variety of therapeutic importance against oxidative stress. MAIN METHODS: This study was designed to assess potential role of polyphenolic compounds in neurocognitive functions and prevention against oxidative stress. For this purpose, young rats were orally treated with naringenin (NAR), curcumin (CUR) and quercetin (QUE) at a dose of 50mg/kg, 200mg/kg and 50mg/kg respectively for 16days. At 4th day of drug administration cognitive functions were monitored by Morris water maze (MWM) test. In MWM cognitive functions in terms of learning acquisition (1h after training), retention (24h after training), memory extinction (4days after training), and reconsolidation (8 and 12days after training) were monitored. Biochemical and neurochemical analysis were done in whole brain. KEY FINDINGS: Treatment of NAR, CUR and QUE significantly enhanced learning acquisition, memory retention and reconsolidation and prevented memory extinction. Treatment of NAR and QUE prevented the alteration of brain antioxidant defence system by enhancing antioxidant enzyme activities and increasing antioxidant compound concentration. Oxidative stress in terms of lipid peroxidation was significantly prevented in treated rats. Serotonergic and cholinergic improvement was also found in treated rats. SIGNIFICANCE: The present study therefore provides biological evidence supporting the usefulness of these polyphenolic compounds in daily life for improvement of cognitive abilities and hence may have a potential role in the management of dementia and related disorders.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Cognição/efeitos dos fármacos
Curcumina/farmacologia
Flavanonas/farmacologia
Memória/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Quercetina/farmacologia
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Acetilcolinesterase/metabolismo
Animais
Antioxidantes/administração & dosagem
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Colinérgicos/farmacologia
Curcumina/administração & dosagem
Flavanonas/administração & dosagem
Masculino
Quercetina/administração & dosagem
Ratos
Ratos Wistar
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cholinergic Agents); 0 (Flavanones); 333DO1RDJY (Serotonin); 9IKM0I5T1E (Quercetin); EC 3.1.1.7 (Acetylcholinesterase); HN5425SBF2 (naringenin); IT942ZTH98 (Curcumin); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  2 / 1867 MEDLINE  
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[PMID]:28800459
[Au] Autor:Wang J; Cai P; Yang XL; Li F; Wu JJ; Kong LY; Wang XB
[Ad] Endereço:Jiangsu Key Laboratory of Bioactive Natural Product Research, State Key Laboratory of Natural Medicines, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, People's Republic of China.
[Ti] Título:Novel cinnamamide-dibenzylamine hybrids: Potent neurogenic agents with antioxidant, cholinergic, and neuroprotective properties as innovative drugs for Alzheimer's disease.
[So] Source:Eur J Med Chem;139:68-83, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:By using fragments endowed with interesting and complementary properties for the treatment of Alzheimer's disease (AD), a novel series of cinnamamide-dibenzylamine hybrids have been designed, synthesized, and evaluated biologically. In vitro assay indicated that most of the target compounds exhibited a significant ability to inhibit ChEs, strong potency inhibitory of self-induced ß-amyloid (Aß) aggregation and to act as potential antioxidants and biometal chelators. A Lineweaver-Burk plot and molecular modeling study showed that compound 7f targeted both the CAS and PAS of AChE. In addition, compound 7f could chelate metal ions, reduce PC12 cells death induced by oxidative stress and penetrate the blood-brain barrier (BBB). Overall, all of these outstanding in vitro results in combination with promising in vivo outcomes highlighted derivative 7f as the lead structure worthy of further investigation.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Antioxidantes/farmacologia
Benzilaminas/farmacologia
Colinérgicos/farmacologia
Inibidores da Colinesterase/farmacologia
Cinamatos/farmacologia
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Antioxidantes/síntese química
Antioxidantes/química
Benzilaminas/química
Barreira Hematorretiniana/efeitos dos fármacos
Butirilcolinesterase/metabolismo
Morte Celular/efeitos dos fármacos
Colinérgicos/síntese química
Colinérgicos/química
Inibidores da Colinesterase/síntese química
Inibidores da Colinesterase/química
Cinamatos/química
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Fármacos Neuroprotetores/síntese química
Fármacos Neuroprotetores/química
Estresse Oxidativo/efeitos dos fármacos
Células PC12
Ratos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzylamines); 0 (Cholinergic Agents); 0 (Cholinesterase Inhibitors); 0 (Cinnamates); 0 (Neuroprotective Agents); 3G0YFX01C6 (dibenzylamine); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase); Y0JET56H7N (cinnamamide)
[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:170812
[St] Status:MEDLINE


  3 / 1867 MEDLINE  
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[PMID]:28791707
[Au] Autor:Prado MAM; Marchot P; Silman I
[Ad] Endereço:Robarts Research Institute, Department of Physiology and Pharmacology and Department of Anatomy and Cell Biology, The University of Western Ontario London, Ontario, Canada.
[Ti] Título:Preface: Cholinergic Mechanisms.
[So] Source:J Neurochem;142 Suppl 2:3-6, 2017 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This special issue is a companion to the meeting 'XVth International Symposium on Cholinergic Mechanisms', and is edited by Israel Silman, Marco Prado and Pascale Marchot. In the review articles, renowned researchers in the field capture key mechanisms of cholinergic neurotransmission, from genomic amplification of cholinesterase genes, splicing and post-translational modifications; features of the neuromuscular junction, implications of cholinergic circuitry that are relevant to addiction, anxiety and mood, to preclinical models, protein biomarkers, and clinical findings that are relevant to pathology, for example, developmental neurotoxicity. The broad variety of features reflects the impact of cholinergic mechanisms on many physiological events and emphasizes the importance of research in this area. This is the Preface for the special issue XVth International Symposium on Cholinergic Mechanisms.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Colinérgicos/farmacologia
Junção Neuromuscular/metabolismo
Síndromes Neurotóxicas/metabolismo
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Aditivo/tratamento farmacológico
Comportamento Aditivo/fisiopatologia
Seres Humanos
Síndromes Neurotóxicas/tratamento farmacológico
Transmissão Sináptica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholinergic Agents); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14027


  4 / 1867 MEDLINE  
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[PMID]:28791706
[Au] Autor:Haam J; Yakel JL
[Ad] Endereço:Neurobiology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC, USA.
[Ti] Título:Cholinergic modulation of the hippocampal region and memory function.
[So] Source:J Neurochem;142 Suppl 2:111-121, 2017 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acetylcholine (ACh) plays an important role in memory function and has been implicated in aging-related dementia, in which the impairment of hippocampus-dependent learning strongly manifests. Cholinergic neurons densely innervate the hippocampus, mediating the formation of episodic as well as semantic memory. Here, we will review recent findings on acetylcholine's modulation of memory function, with a particular focus on hippocampus-dependent learning, and the circuits involved. In addition, we will discuss the complexity of ACh actions in memory function to better understand the physiological role of ACh in memory. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Colinérgicos/farmacologia
Hipocampo/efeitos dos fármacos
Memória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Envelhecimento/fisiologia
Animais
Hipocampo/metabolismo
Seres Humanos
Aprendizagem/fisiologia
Memória/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholinergic Agents); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14052


  5 / 1867 MEDLINE  
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[PMID]:28791705
[Au] Autor:Anglister L; Cherniak M; Lev-Tov A
[Ad] Endereço:Department of Medical Neurobiology, IMRIC, the Hebrew University-Hadassah Medical School, Jerusalem, Israel.
[Ti] Título:Ascending pathways that mediate cholinergic modulation of lumbar motor activity.
[So] Source:J Neurochem;142 Suppl 2:82-89, 2017 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Deciphering neuronal pathways that reactivate spinal central pattern generators (CPGs) and modulate the activity of spinal motoneurons in mammals in the absence of supraspinal control is important for understanding of neural control of movement and for developing novel therapeutic approaches to improve the mobility of spinal cord injury patients. Previously, we showed that the sacral and lumbar cholinergic system could potently modulate the locomotor CPGs in newborn rodents. Here, we review these and our more recent studies of sacral relay neurons with lumbar projections to the locomotor CPGs and to lumbar motoneurons and demonstrate that sacral and lumbar cholinergic components have the capacity to control the frequency of the locomotor CPGs and at the same time the motor output of the activated lumbar motoneurons during motor behavior. A model describing the suggested ascending sacro-lumbar connectivity involved in modulation of the locomotor rhythm by sacral cholinergic components is proposed and discussed. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
[Mh] Termos MeSH primário: Acetilcolina/farmacologia
Colinérgicos/farmacologia
Locomoção/efeitos dos fármacos
Vértebras Lombares/efeitos dos fármacos
Atividade Motora/efeitos dos fármacos
Neurônios Motores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Animais
Seres Humanos
Locomoção/fisiologia
Atividade Motora/fisiologia
Neurônios Motores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholinergic Agents); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14065


  6 / 1867 MEDLINE  
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[PMID]:28625954
[Au] Autor:Batool Z; Agha F; Ahmad S; Liaquat L; Tabassum S; Khaliq S; Anis L; Sajid I; Emad S; Perveen T; Haider S
[Ad] Endereço:Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Pakistan.
[Ti] Título:Attenuation of cadmium-induced decline in spatial, habituation and recognition memory by long-term administration of almond and walnut supplementation: Role of cholinergic function.
[So] Source:Pak J Pharm Sci;30(1 Suppl):273-279, 2017 Jan.
[Is] ISSN:1011-601X
[Cp] País de publicação:Pakistan
[La] Idioma:eng
[Ab] Resumo:Excessive exposure of cadmium which is regarded as a neurotoxin can stimulate aging process by inducing abnormality in neuronal function. It has been reported that supplementation of almond and walnut attenuate age-related memory loss. Present study was designed to investigate the weekly administration of cadmium for one month on learning and memory function with relation to cholinergic activity. Cadmium was administered at the dose of 50 mg/kg/week. Whereas, almond and walnut was supplemented at the dose of 400 mg/kg/day along with cadmium administration to separate set of rats. At the end of experiment, memory function was assessed by Morris water maze, open field test and novel object recognition test. Results of the present study showed that cadmium administration significantly reduced memory retention. Reduced acetylcholine levels and elevated acetyl cholinesterase activity were also observed in frontal cortex and hippocampus of cadmium treated rats. Malondialdehyde levels were also significantly increased following the administration of cadmium. Daily supplementation of almond and walnut for 28 days significantly attenuated cadmium-induced memory impairment in rats. Results of the present study are discussed in term of cholinergic activity in cadmium-induced memory loss and its attenuation by nuts supplementation in rats.
[Mh] Termos MeSH primário: Cádmio/administração & dosagem
Colinérgicos/administração & dosagem
Habituação Psicofisiológica/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Transtornos da Memória/induzido quimicamente
Transtornos da Memória/dietoterapia
Memória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Envelhecimento/efeitos dos fármacos
Animais
Suplementos Nutricionais
Juglans
Aprendizagem em Labirinto/efeitos dos fármacos
Prunus dulcis
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agents); 00BH33GNGH (Cadmium); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


  7 / 1867 MEDLINE  
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[PMID]:28581010
[Au] Autor:Shiao YJ; Su MH; Lin HC; Wu CR
[Ad] Endereço:National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei, Taiwan.
[Ti] Título:Echinacoside ameliorates the memory impairment and cholinergic deficit induced by amyloid beta peptides via the inhibition of amyloid deposition and toxicology.
[So] Source:Food Funct;8(6):2283-2294, 2017 Jun 01.
[Is] ISSN:2042-650X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Echinacoside is a phenylethanoid glycoside and possesses neuroprotective activity in vitro and in vivo. This study investigates the role of the amyloid cascade and central neuronal function on the protective effects of echinacoside in amyloid ß peptide 1-42 (Aß 1-42)-treated SH-SY5Y cells and an Aß 1-42-infused rat. Echinacoside inhibited Aß 1-42 oligomerization in vitro and restored the cell viability that was reduced by Aß 1-42 in SH-SY5Y cells. Intracisternal infusion with Aß 1-42 by an osmotic pump caused cognitive deficits, an increase in amyloid deposition and acetylcholinesterase activities, and a decrease in the brain's levels of acetylcholine and dopamine. Echinacoside reduced the cognitive deficits and amyloid deposition, and it reversed the cortical cholinergic dysfunction that was caused by Aß 1-42 in rats. Echinacoside further reversed the memory impairment in the Morris water maze task caused by scopolamine in mice. Therefore, we suggest that echinacoside ameliorated cognitive dysfunction that was caused by Aß 1-42 by blocking amyloid deposition via inhibiting amyloid oligomerization and reversing the cortical cholinergic neuronal function via decreasing amyloid neurotoxicity.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/metabolismo
Glicosídeos/administração & dosagem
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Acetilcolinesterase/metabolismo
Doença de Alzheimer/enzimologia
Doença de Alzheimer/metabolismo
Doença de Alzheimer/psicologia
Peptídeos beta-Amiloides/química
Peptídeos beta-Amiloides/toxicidade
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Colinérgicos/administração & dosagem
Seres Humanos
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Memória/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos ICR
Ratos
Ratos Sprague-Dawley
Hidrobrometo de Escopolamina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Cholinergic Agents); 0 (Glycosides); 451IFR0GXB (Scopolamine Hydrobromide); EC 3.1.1.7 (Acetylcholinesterase); I04O1DT48T (echinacoside); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1039/c7fo00267j


  8 / 1867 MEDLINE  
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[PMID]:28521121
[Au] Autor:Gais S; Schönauer M
[Ad] Endereço:Institute of Medical Psychology and Behavioral Neurobiology, University of Tübingen, 72076 Tübingen, Germany. Electronic address: steffen.gais@uni-tuebingen.de.
[Ti] Título:Untangling a Cholinergic Pathway from Wakefulness to Memory.
[So] Source:Neuron;94(4):696-698, 2017 May 17.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acetylcholine is a major modulator of learning and memory, and its availability varies across the sleep-wake cycle. In this issue of Neuron, Papouin et al. (2017) describe a D-serine-dependent pathway involving astroglia by which the transmitter tunes the hippocampus toward memory encoding during wakefulness.
[Mh] Termos MeSH primário: Sono
Vigília
[Mh] Termos MeSH secundário: Acetilcolina
Colinérgicos
Seres Humanos
Memória
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agents); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE


  9 / 1867 MEDLINE  
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[PMID]:28440734
[Au] Autor:Wu J; Jiao ZY; Li RZ; Lu HL; Zhang HH; Cianflone K
[Ad] Endereço:1 Department of Pediatrics, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
[Ti] Título:Cholinergic activation suppresses palmitate-induced macrophage activation and improves acylation stimulating protein resistance in co-cultured adipocytes.
[So] Source:Exp Biol Med (Maywood);242(9):961-973, 2017 May.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acylation-stimulating protein (ASP), produced through activation of the alternative complement immune system, modulates lipid metabolism. Using a trans-well co-culture cell model, the mitigating role of α7-nicotinic acetylcholine receptor (α7nAChR)-mediated cholinergic pathway on ASP resistance was evaluated. ASP signaling in adipocytes via its receptor C5L2 and signaling intermediates Gαq, Gß, phosphorylated protein kinase C-α, and protein kinase C-ζ were markedly suppressed in the presence of TNFα or medium from palmitate-treated RAW264.7 macrophages, indicating ASP resistance. There was no direct effect of α7nAChR activation in 3T3-L1 cell culture. However, α7nAChR activation almost completely reversed the ASP resistance in adipocytes co-cultured with palmitate-treated RAW264.7 macrophages. Further, α7nAChR activation could suppress the production of pro-inflammatory molecules TNFα and interleukin-6 produced from palmitate-treated co-cultured macrophages. These results suggest that macrophages play a significant role in the pathogenesis of ASP resistance and α7nAChR activation secondarily improves adipose ASP resistance through suppression of inflammation in macrophages. Impact statement 1. Adipocyte-macrophage interaction in acylation-stimulating protein (ASP) resistance 2. Lipotoxicity induced inflammatory response in ASP resistance 3. A vicious circle between lipotoxicity and inflammatory response in ASP resistance 4. Cholinergic modulation of inflammatory response in adipocyte and macrophage.
[Mh] Termos MeSH primário: Adipócitos/fisiologia
Colinérgicos/metabolismo
Complemento C3a/metabolismo
Ativação de Macrófagos/efeitos dos fármacos
Palmitatos/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Técnicas de Cocultura
Camundongos
Receptor Nicotínico de Acetilcolina alfa7/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agents); 0 (Palmitates); 0 (alpha7 Nicotinic Acetylcholine Receptor); 0 (complement C3a, des-Arg-(77)-); 80295-42-7 (Complement C3a)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217700522


  10 / 1867 MEDLINE  
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[PMID]:28427894
[Au] Autor:Nardone R; Trinka E
[Ad] Endereço:Department of Neurology, Franz Tappeiner Hospital, Merano, Italy; Department of Neurology, Christian Doppler Klinik, Paracelsus Medical University, Salzburg, Austria. Electronic address: raffaele.nardone@asbmeran-o.it.
[Ti] Título:In vivo evaluation of central cholinergic circuits in Parkinson's disease using transcranial magnetic stimulation.
[So] Source:Clin Neurophysiol;128(6):1028-1029, 2017 06.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença de Parkinson
Estimulação Magnética Transcraniana
[Mh] Termos MeSH secundário: Colinérgicos
Potencial Evocado Motor
Seres Humanos
Córtex Motor
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Cholinergic Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE



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