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Pesquisa : D02.455.426.100.050.035.500 [Categoria DeCS]
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  1 / 1958 MEDLINE  
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[PMID]:29407462
[Au] Autor:Zambrano P; Suwalsky M; Jemiola-Rzeminska M; Strzalka K
[Ad] Endereço:Faculty of Chemical Sciences, University of Concepción, Concepción, Chile. Electronic address: pzambranol@udec.cl.
[Ti] Título:Studies on the interaction of NMDA receptor antagonist memantine with cell membranes: A mini-review.
[So] Source:Chem Biol Interact;283:47-50, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Memantine is an NMDA receptor antagonist clinically used for the treatment of moderate to severe Alzheimer's disease. Currently, it is the only NMDA receptor antagonist drug marketed against this disease. Despite the large number of publications regarding its clinical and therapeutic use, studies related to its mechanism of action are still inconclusive. Knowledge of drug interactions with cell membranes may lead to the development of novel drugs for neurodegenerative diseases. The present mini-review aims to give an overview of the latest findings regarding the interaction of memantine with cell membranes, specifically with that of the human erythrocyte.
[Mh] Termos MeSH primário: Membrana Celular/efeitos dos fármacos
Memantina/farmacologia
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
[Mh] Termos MeSH secundário: Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Membrana Celular/metabolismo
Eritrócitos/citologia
Eritrócitos/efeitos dos fármacos
Eritrócitos/metabolismo
Seres Humanos
Memantina/química
Memantina/uso terapêutico
Microscopia Eletrônica de Varredura
Receptores de N-Metil-D-Aspartato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, N-Methyl-D-Aspartate); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  2 / 1958 MEDLINE  
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[PMID]:27776769
[Au] Autor:Wheate NJ; Dickson KA; Kim RR; Nematollahi A; Macquart RB; Kayser V; Yu G; Church WB; Marsh DJ
[Ad] Endereço:Faculty of Pharmacy, University of Sydney, Sydney, NSW 2006, Australia. Electronic address: nial.wheate@sydney.edu.au.
[Ti] Título:Host-Guest Complexes of Carboxylated Pillar[n]arenes With Drugs.
[So] Source:J Pharm Sci;105(12):3615-3625, 2016 Dec.
[Is] ISSN:1520-6017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pillar[n]arenes are a new family of nanocapsules that have shown application in a number of areas, but because of their poor water solubility their biomedical applications are limited. Recently, a method of synthesizing water-soluble pillar[n]arenes was developed. In this study, carboxylated pillar[n]arenes (WP[n], n = 6 or 7) have been examined for their ability to form host-guest complexes with compounds relevant to drug delivery and biodiagnostic applications. Both pillar[n]arenes form host-guest complexes with memantine, chlorhexidine hydrochloride, and proflavine by H nuclear magnetic resonance and modeling. Binding is stabilized by hydrophobic effects within the cavities, and hydrogen bonding and electrostatic interactions at the portals. Encapsulation within WP[6] results in the complete and efficient quenching of proflavine fluorescence, giving rise to "on" and "off" states that have potential in biodiagnostics. The toxicity of the pillar[n]arenes was examined using in vitro growth assays with the OVCAR-3 and HEK293 cell lines. The pillar[n]arenes are relatively nontoxic to cells except at high doses and after prolonged continuous exposure. Overall, the results show that there could be a potentially large range of medical applications for carboxylated pillar[n]arene nanocapsules.
[Mh] Termos MeSH primário: Substâncias Macromoleculares/metabolismo
Modelos Moleculares
Preparações Farmacêuticas/metabolismo
Compostos de Amônio Quaternário/metabolismo
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Substâncias Macromoleculares/química
Memantina/metabolismo
Preparações Farmacêuticas/química
Proflavina/química
Proflavina/metabolismo
Compostos de Amônio Quaternário/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Macromolecular Substances); 0 (Pharmaceutical Preparations); 0 (Quaternary Ammonium Compounds); CY3RNB3K4T (Proflavine); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  3 / 1958 MEDLINE  
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[PMID]:27776560
[Au] Autor:Veerman SR; Schulte PF; Deijen JB; de Haan L
[Ad] Endereço:Mental Health Service Noord-Holland Noord,Community Mental Health Division,Flexible Assertive Community Treatment,Alkmaar,The Netherlands.
[Ti] Título:Adjunctive memantine in clozapine-treated refractory schizophrenia: an open-label 1-year extension study.
[So] Source:Psychol Med;47(2):363-375, 2017 Jan.
[Is] ISSN:1469-8978
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In a recent placebo-controlled, double-blind crossover trial (n = 52), significant beneficial effects on memory (d = 0.30) and negative symptoms (d = 0.29) were found after 12 weeks of memantine augmentation in patients with clozapine-refractory schizophrenia. In this open-label 1-year extension study we report the long-term effects and tolerability of memantine add-on therapy to clozapine. METHOD: Completers of the first trial who experienced beneficial effects during 12 weeks of memantine treatment received memantine for 1 year. Primary endpoints were memory and executive function using the Cambridge Neuropsychological Test Automated Battery, the Positive and Negative Syndrome Scale (PANSS), and the Clinical Global Impression Severity Scale (CGI-S). RESULTS: Of 31 randomized controlled trial completers who experienced beneficial effects from memantine, 24 received memantine for 1 year. The small improvement in memory found in the memantine condition in the placebo-controlled trial remained stable in the extension study. Executive function did not improve. After 26 weeks of memantine add-on therapy to clozapine, PANSS negative symptoms (r = 0.53), PANSS positive symptoms (r = 0.50) and PANSS total symptoms (r = 0.54) significantly improved. Even further significant improvement in all these measures was observed between 26 weeks and 52 weeks of memantine, with effect sizes varying from 0.39 to 0.51. CGI-S showed a non-significant moderate improvement at 26 weeks (r = 0.36) and 52 weeks (r = 0.34). Memantine was well tolerated without serious adverse effects. CONCLUSIONS: In the 1-year extension phase the favourable effect of adjunctive memantine on memory was sustained and we observed further improvement of negative, positive and overall symptoms in patients with clozapine-treated refractory schizophrenia.
[Mh] Termos MeSH primário: Antipsicóticos/farmacologia
Clozapina/farmacologia
Disfunção Cognitiva/tratamento farmacológico
Antagonistas de Aminoácidos Excitatórios/farmacologia
Função Executiva
Memantina/farmacologia
Transtornos da Memória/tratamento farmacológico
Esquizofrenia/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Disfunção Cognitiva/etiologia
Resistência a Medicamentos
Sinergismo Farmacológico
Quimioterapia Combinada
Antagonistas de Aminoácidos Excitatórios/administração & dosagem
Antagonistas de Aminoácidos Excitatórios/efeitos adversos
Função Executiva/efeitos dos fármacos
Feminino
Seguimentos
Seres Humanos
Masculino
Memantina/administração & dosagem
Memantina/efeitos adversos
Transtornos da Memória/etiologia
Meia-Idade
Esquizofrenia/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Excitatory Amino Acid Antagonists); J60AR2IKIC (Clozapine); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1017/S0033291716002476


  4 / 1958 MEDLINE  
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[PMID]:28922421
[Au] Autor:Rahman A; Lamberty Y; Schenker E; Cella M; Languille S; Bordet R; Richardson J; Pifferi F; Aujard F
[Ad] Endereço:UMR 7179 Centre National de la Recherche Scientifique, Muséum National d'Histoire Naturelle, Brunoy, France.
[Ti] Título:Effects of acute administration of donepezil or memantine on sleep-deprivation-induced spatial memory deficit in young and aged non-human primate grey mouse lemurs (Microcebus murinus).
[So] Source:PLoS One;12(9):e0184822, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of novel therapeutics to prevent cognitive decline of Alzheimer's disease (AD) is facing paramount difficulties since the translational efficacy of rodent models did not resulted in better clinical results. Currently approved treatments, including the acetylcholinesterase inhibitor donepezil (DON) and the N-methyl-D-aspartate antagonist memantine (MEM) provide marginal therapeutic benefits to AD patients. There is an urgent need to develop a predictive animal model that is phylogenetically proximal to humans to achieve better translation. The non-human primate grey mouse lemur (Microcebus murinus) is increasingly used in aging research, but there is no published results related to the impact of known pharmacological treatments on age-related cognitive impairment observed in this primate. In the present study we investigated the effects of DON and MEM on sleep-deprivation (SD)-induced memory impairment in young and aged male mouse lemurs. In particular, spatial memory impairment was evaluated using a circular platform task after 8 h of total SD. Acute single doses of DON or MEM (0.1 and 1mg/kg) or vehicle were administered intraperitoneally 3 h before the cognitive task during the SD procedure. Results indicated that both doses of DON were able to prevent the SD-induced deficits in retrieval of spatial memory as compared to vehicle-treated animals, both in young and aged animals Likewise, MEM show a similar profile at 1 mg/kg but not at 0.1mg/kg. Taken together, these results indicate that two widely used drugs for mitigating cognitive deficits in AD were partially effective in sleep deprived mouse lemurs, which further support the translational potential of this animal model. Our findings demonstrate the utility of this primate model for further testing cognitive enhancing drugs in development for AD or other neuropsychiatric conditions.
[Mh] Termos MeSH primário: Envelhecimento/efeitos dos fármacos
Indanos/farmacologia
Memantina/farmacologia
Transtornos da Memória/tratamento farmacológico
Piperidinas/farmacologia
Privação do Sono/tratamento farmacológico
Memória Espacial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doença de Alzheimer/complicações
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/fisiopatologia
Animais
Cheirogaleidae
Modelos Animais de Doenças
Masculino
Transtornos da Memória/etiologia
Transtornos da Memória/fisiopatologia
Privação do Sono/complicações
Privação do Sono/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indans); 0 (Piperidines); 8SSC91326P (donepezil); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184822


  5 / 1958 MEDLINE  
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[PMID]:28917837
[Au] Autor:Takahashi-Ito K; Makino M; Okado K; Tomita T
[Ad] Endereço:Venture Science Laboratories, R&D Division, Daiichi-Sankyo Co. Ltd., Shinagawa-ku, Tokyo 140-8710, Japan. Electronic address: takahashi.kaori.ne@daiichisankyo.co.jp.
[Ti] Título:Memantine inhibits ß-amyloid aggregation and disassembles preformed ß-amyloid aggregates.
[So] Source:Biochem Biophys Res Commun;493(1):158-163, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memantine, an uncompetitive glutamatergic N-methyl-d-aspartate (NMDA) receptor antagonist, is widely used as a medication for the treatment of Alzheimer's disease (AD). We previously reported that chronic treatment of AD with memantine reduces the amount of insoluble ß-amyloid (Aß) and soluble Aß oligomers in animal models of AD. The mechanisms by which memantine reduces Aß levels in the brain were evaluated by determining the effect of memantine on Aß aggregation using thioflavin T and transmission electron microscopy. Memantine inhibited the formation of Aß(1-42) aggregates in a concentration-dependent manner, whereas amantadine, a structurally similar compound, did not affect Aß aggregation at the same concentrations. Furthermore, memantine inhibited the formation of different types of Aß aggregates, including Aßs carrying familial AD mutations, and disaggregated preformed Aß(1-42) fibrils. These results suggest that the inhibition of Aß aggregation and induction of Aß disaggregation may be involved in the mechanisms by which memantine reduces Aß deposition in the brain.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/química
Peptídeos beta-Amiloides/ultraestrutura
Memantina/química
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/ultraestrutura
[Mh] Termos MeSH secundário: Dimerização
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Peptide Fragments); 0 (amyloid beta-protein (1-42)); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


  6 / 1958 MEDLINE  
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[PMID]:28877967
[Au] Autor:Glasgow NG; Povysheva NV; Azofeifa AM; Johnson JW
[Ad] Endereço:Department of Neuroscience and Center for Neuroscience and.
[Ti] Título:Memantine and Ketamine Differentially Alter NMDA Receptor Desensitization.
[So] Source:J Neurosci;37(40):9686-9704, 2017 Oct 04.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memantine and ketamine are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with similar potency and kinetics, but display vastly different clinical profiles. This discrepancy has been hypothesized to result from inhibition by memantine and ketamine of overlapping but distinct NMDAR subpopulations. For example, memantine but not ketamine may inhibit extrasynaptic NMDARs more effectively than synaptic NMDARs. However, the basis for preferential NMDAR inhibition depending on subcellular location has not been investigated systematically. We integrated recordings from heterologously expressed single NMDAR subtypes, kinetic modeling, and recordings of synaptically evoked NMDAR responses in acute brain slices to investigate mechanisms by which channel blockers may distinguish NMDAR subpopulations. We found that memantine and ketamine differentially alter NMDAR desensitization and that memantine stabilizes a Ca -dependent desensitized state. As a result, inhibition by memantine of GluN1/2A receptors in tsA201 cells and of native synaptic NMDARs in cortical pyramidal neurons from mice of either sex increased in conditions that enhanced intracellular Ca accumulation. Therefore, differential inhibition by memantine and ketamine based on NMDAR location is likely to result from location dependence of the intensity and duration of NMDAR activation. Modulation of Ca -dependent NMDAR desensitization is an unexplored mechanism of inhibitory action with the potential to endow drugs with NMDAR selectivity that leads to superior clinical profiles. Our results suggest that designing compounds to target specific receptor states, rather than specific receptor types, may be a viable strategy for future drug development. Memantine and ketamine are NMDA receptor (NMDAR) channel-blocking drugs with divergent clinical effects. Understanding mechanistically their differential actions may advance our understanding of nervous system disorders and suggest strategies for the design of more effective drugs. Here, we show that memantine and ketamine have contrasting effects on NMDAR desensitization. Ketamine binding decreases occupancy of desensitized states of the GluN1/2B NMDAR subtype. In contrast, memantine binding increases occupancy of GluN1/2A and native NMDAR desensitized states entered after accumulation of intracellular Ca , a novel inhibitory mechanism. These properties may contribute to inhibition of distinct NMDAR subpopulations by memantine and ketamine and help to explain their differential clinical effects. Our results suggest stabilization of Ca -dependent desensitized states as a new strategy for pharmaceutical neuroprotection.
[Mh] Termos MeSH primário: Ketamina/farmacologia
Memantina/farmacologia
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/metabolismo
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Células HEK293
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Cultura de Órgãos
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (Gprin1 protein, mouse); 0 (NR2B NMDA receptor); 0 (Nerve Tissue Proteins); 0 (Receptors, N-Methyl-D-Aspartate); 690G0D6V8H (Ketamine); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171021
[Lr] Data última revisão:
171021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1173-17.2017


  7 / 1958 MEDLINE  
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[PMID]:28855009
[Au] Autor:Glynn-Servedio BE; Ranola TS
[Ti] Título:AChE Inhibitors and NMDA Receptor Antagonists in Advanced Alzheimer's Disease.
[So] Source:Consult Pharm;32(9):511-518, 2017 Sep 01.
[Is] ISSN:0888-5109
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of this article is to review the available evidence for duration of treatment with, and considerations for discontinuation of, acetylcholinesterase inhibitors and N-methyl-d-aspartate receptor antagonists in Alzheimer's disease. DATA SOURCES: Literature searches of clinical trials and meta-analyses were conducted using PubMed with the search terms Alzheimer's, dementia, donepezil, galantamine, memantine, and rivastigmine. References from included trials were also used to find additional citations. STUDY SELECTION/DATA EXTRACTION: 2,925 articles were initially identified. Twenty-one studies were included that looked at the use of acetylcholinesterase inhibitors and/or memantine in the treatment of moderate-to-severe Alzheimer's dementia. DATA SYNTHESIS: Several clinical trials have demonstrated small improvements in measures of cognition and activities of daily living with medications used to treat dementia. However, not all patients will benefit from treatment, and the impact of treatment on long-term outcomes, including institutionalization, remains unclear. This paper reviews the available data to support the use of acetylcholinesterase inhibitors and/or memantine in patients with advanced Alzheimer's disease, including those in nursing facilities, and reviews recommendations for consideration of therapy discontinuation. CONCLUSION: The evidence to support a specific time frame for discontinuation of Alzheimer's disease treatment is limited. It is reasonable to stop a medication if there is no noticeable benefit after the first three months of treatment or once a patient's dementia progresses to a point where there would be no meaningful benefit from continued therapy.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Inibidores da Colinesterase/uso terapêutico
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
[Mh] Termos MeSH secundário: Atividades Cotidianas
Ensaios Clínicos como Assunto
Seres Humanos
Memantina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (Receptors, N-Methyl-D-Aspartate); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.4140/TCP.n.2017.511


  8 / 1958 MEDLINE  
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[PMID]:28827830
[Au] Autor:Chen R; Chan PT; Chu H; Lin YC; Chang PC; Chen CY; Chou KR
[Ad] Endereço:School of Nursing, College of Nursing, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:Treatment effects between monotherapy of donepezil versus combination with memantine for Alzheimer disease: A meta-analysis.
[So] Source:PLoS One;12(8):e0183586, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This is the first meta-analysis to compare the treatment effects and safety of administering donepezil alone versus a combination of memantine and donepezil to treat patients with moderate to severe Alzheimer Disease, particularly regarding cognitive functions, behavioral and psychological symptoms in dementia (BPSD), and global functions. METHODS: PubMed, Medline, Embase, PsycINFO, and Cochrane databases were used to search for English and non-English articles for inclusion in the meta-analysis to evaluate the effect size and incidence of adverse drug reactions of different treatments. RESULTS: Compared with patients who received donepezil alone, those who received donepezil in combination with memantine exhibited limited improvements in cognitive functions (g = 0.378, p < .001), BPSD (g = -0.878, p < .001) and global functions (g = -0.585, p = .004). Gradual titration of memantine plus a fixed dose and gradual titration of donepezil as well as a fixed dose and gradual titration of memantine resulted in limited improvements in cognitive functions(g = 0.371, p = .005), BPSD(g = -0.913, p = .001), and global functions(g = -0.371, p = .001). CONCLUSION: Both in the 24th week and at the final evaluation point, the combination of donepezil and memantine led to greater improvement in cognitive functions, BPSD, and global functions than did donepezil alone in patients with moderate to severe Alzheimer Disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Indanos/uso terapêutico
Memantina/uso terapêutico
Nootrópicos/uso terapêutico
Piperidinas/uso terapêutico
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Seres Humanos
Indanos/administração & dosagem
Memantina/administração & dosagem
Nootrópicos/administração & dosagem
Piperidinas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Indans); 0 (Nootropic Agents); 0 (Piperidines); 8SSC91326P (donepezil); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183586


  9 / 1958 MEDLINE  
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[PMID]:28632848
[Au] Autor:Bögli SY; Afthinos M; Huang MY
[Ad] Endereço:Department of Neurology, University Hospital Zurich, University of Zurich, Switzerland.
[Ti] Título:Effect of Gabapentin/Memantine on the Infantile Nystagmus Syndrome in the Zebrafish Model: Implications for the Therapy of Ocular Motor Diseases.
[So] Source:Invest Ophthalmol Vis Sci;58(7):3149-3157, 2017 Jun 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Infantile nystagmus syndrome (INS) is a disorder characterized by typical horizontal eye oscillations. Due to the uncertain etiology of INS, developing specific treatments remains difficult. Single reports demonstrated, on limited measures, alleviating effects of gabapentin and memantine. In the current study, we employed the zebrafish INS model belladonna (bel) to conduct an in-depth study of how gabapentin and memantine interventions alleviate INS signs, which may further restore visual conditions in affected subjects. Moreover, we described the influence of both medications on ocular motor functions in healthy zebrafish, evaluating possible iatrogenic effects. Methods: Ocular motor function and INS characteristics were assessed by eliciting optokinetic response, spontaneous nystagmus, and spontaneous saccades in light and in dark, in 5- to 6-day postfertilization bel larvae and heterozygous siblings. Single larvae were recorded before and after a 1-hour drug treatment (200 mM gabapentin/0.2 mM memantine). Results: Both interventions significantly reduced nystagmus intensity (gabapentin: 59.98%, memantine: 39.59%). However, while the application of gabapentin affected all tested ocular motor functions, memantine specifically reduced nystagmus amplitude and intensity, and thus left controls completely unaffected. Finally, both drug treatments resulted in specific changes in nystagmus waveform and velocity. Conclusions: Our study provides deeper insight into gabapentin and memantine treatment effect in the zebrafish INS model. Moreover, this study should establish zebrafish as a pharmacologic animal model for treating nystagmus and ocular motor disease, serving as a basis for future large-scale drug screenings.
[Mh] Termos MeSH primário: Aminas/farmacologia
Ácidos Cicloexanocarboxílicos/farmacologia
Movimentos Oculares/fisiologia
Memantina/farmacologia
Nistagmo Congênito/tratamento farmacológico
Ácido gama-Aminobutírico/farmacologia
[Mh] Termos MeSH secundário: Animais
Bloqueadores dos Canais de Cálcio/farmacologia
Modelos Animais de Doenças
Antagonistas de Aminoácidos Excitatórios/farmacologia
Movimentos Oculares/efeitos dos fármacos
Nistagmo Congênito/fisiopatologia
Síndrome
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (Calcium Channel Blockers); 0 (Cyclohexanecarboxylic Acids); 0 (Excitatory Amino Acid Antagonists); 56-12-2 (gamma-Aminobutyric Acid); 6CW7F3G59X (gabapentin); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21308


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[PMID]:28534431
[Au] Autor:Ahmed AS; Elgharabawy RM; Al-Najjar AH
[Ad] Endereço:1 Pharmacology and Toxicology Department, Faculty of Pharmacy, Qassim University, KSA 51431, Saudi Arabia.
[Ti] Título:Ameliorating effect of anti-Alzheimer's drugs on the bidirectional association between type 2 diabetes mellitus and Alzheimer's disease.
[So] Source:Exp Biol Med (Maywood);242(13):1335-1344, 2017 Jul.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mild to severe forms of nervous system damage were exhibited by approximately 60-70% of diabetics. It is important to understand the association between type 2 diabetes mellitus and Alzheimer's disease. The aim of the present work is to understand the bidirectional association between type 2 diabetes and Alzheimer's disease pathogenesis, that was monitored by glycaemic status, lipid profile, amyloid beta 40 and 42 (Aß40 and Aß42), C-reactive protein, total creatine kinase, total lactate dehydrogenase, D-dimer and magnesium measurements, to assess the association between theses biochemical markers and each other, to estimate the possibility of utilizing the amyloid beta as biochemical marker of T2D in Alzheimer's patients, and to evaluate the effect of piracetam and memantine drugs on diabetes mellitus. This study involved 120 subjects divided into 20 healthy control (group I), 20 diabetic patients (group II), 20 Alzheimer's patients (group III), 20 diabetic Alzheimer's patients with symptomatic treatment (group IV), 20 diabetic Alzheimer's patients treated with memantine (group V), and 20 diabetic Alzheimer's patients treated with piracetam (group VI). The demographic characteristics, diabetic index, and lipid profile were monitored. Plasma amyloid beta 40 and amyloid beta 42, C-reactive protein, total creatine kinase, total lactate dehydrogenase, D-dimer, and magnesium were assayed. The levels of amyloid beta 40 and amyloid beta 42 were significantly elevated in diabetic Alzheimer's patients with symptomatic treatment (group IV) compared to group II (by 50.5 and 7.5 fold, respectively) and group III (by 25.4 and 2.8 fold, respectively). In groups II, III, IV, V and VI, significant and positive associations were monitored between insulin and amyloid beta 40, amyloid beta 42, C-reactive protein, total creatine kinase, and D-dimer. Diabetic markers were significantly decreased in diabetic Alzheimer's patients treated with anti-Alzheimer's drugs (especially piracetam) compared to group IV. This study reveals the role of amyloid beta 40, amyloid beta 42, insulin, HbA1c, lipid profile disturbance, C-reactive protein, D-dimer, and magnesium in the bidirectional correlation between T2D and pathogenesis of Alzheimer's disease, that is powered by their correlations, and therefore the possibility of utilizing Aß as a biochemical marker of T2D in Alzheimer's patients is recommended. Impact statement Several aspects associated with T2D that contribute to AD and vice versa were investigated in this study. Additionally, this work reveals the role of Aß40, Aß42, insulin, HbA1c, lipid profile disturbance, CRP, D-dimer, and magnesium in the bidirectional association between T2D and the pathogenesis of AD, that is powered by their correlations, and therefore the possibility of utilizing Aß as a biochemical marker of T2D in Alzheimer's patients is recommended. Furthermore, the ameloriating effect of anti-Alzheimer's drugs on diabetes mellitus confirms this association. Hereafter, a new approach for treating insulin resistance and diabetes may be developed by new therapeutic potentials such as neutralization of Aß by anti-Aß antibodies.
[Mh] Termos MeSH primário: Doença de Alzheimer/complicações
Doença de Alzheimer/tratamento farmacológico
Biomarcadores/sangue
Diabetes Mellitus Tipo 2/complicações
Memantina/administração & dosagem
Fármacos Neuroprotetores/administração & dosagem
Piracetam/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/patologia
Diabetes Mellitus Tipo 2/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Neuroprotective Agents); W8O17SJF3T (Memantine); ZH516LNZ10 (Piracetam)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217711440



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