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[PMID]:29318278
[Au] Autor:Atri A; Frölich L; Ballard C; Tariot PN; Molinuevo JL; Boneva N; Windfeld K; Raket LL; Cummings JL
[Ad] Endereço:Ray Dolby Brain Health Center, California Pacific Medical Center, San Francisco.
[Ti] Título:Effect of Idalopirdine as Adjunct to Cholinesterase Inhibitors on Change in Cognition in Patients With Alzheimer Disease: Three Randomized Clinical Trials.
[So] Source:JAMA;319(2):130-142, 2018 01 09.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: New therapeutic approaches for Alzheimer disease (AD) are needed. Objective: To assess whether idalopirdine, a selective 5-hydroxytryptamine-6 receptor antagonist, is effective for symptomatic treatment of mild to moderate AD. Design, Setting, and Participants: Three randomized clinical trials that included 2525 patients aged 50 years or older with mild to moderate AD (study 1: n = 933 patients at 119 sites; study 2: n = 858 at 158 sites; and study 3: n = 734 at 126 sites). The 24-week studies were conducted from October 2013 to January 2017; final follow-up on January 12, 2017. Interventions: Idalopirdine (10, 30, or 60 mg/d) or placebo added to cholinesterase inhibitor treatment (donepezil in studies 1 and 2; donepezil, rivastigmine, or galantamine in study 3). Main Outcomes and Measures: Primary end point in all 3 studies: change in cognition total score (range, 0-70; a lower score indicates less impairment) from baseline to 24 weeks measured by the 11-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-Cog); key secondary end points: Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change Scale and 23-item Activities of Daily Living Inventory scores. Dose group efficacy required a significant benefit over placebo for the primary end point and 1 or more key secondary end points. Safety data and adverse event profiles were recorded. Results: Among 2525 patients randomized in the 3 trials (mean age, 74 years; mean baseline ADAS-Cog total score, 26; between 62% and 65% of participants were women), 2254 (89%) completed the studies. In study 1, the mean change in ADAS-Cog total score between baseline and 24 weeks was 0.37 for the 60-mg dose of idalopirdine group, 0.61 for the 30-mg dose group, and 0.41 for the placebo group (adjusted mean difference vs placebo, 0.05 [95% CI, -0.88 to 0.98] for the 60-mg dose group and 0.33 [95% CI, -0.59 to 1.26] for the 30-mg dose group). In study 2, the mean change in ADAS-Cog total score between baseline and 24 weeks was 1.01 for the 30-mg dose of idalopirdine group, 0.53 for the 10-mg dose group, and 0.56 for the placebo group (adjusted mean difference vs placebo, 0.63 [95% CI, -0.38 to 1.65] for the 30-mg dose group; given the gated testing strategy and the null findings at the 30-mg dose, statistical comparison of the 10-mg dose was not performed). In study 3, the mean change in ADAS-Cog total score between baseline and 24 weeks was 0.38 for the 60-mg dose of idalopirdine group and 0.82 for the placebo group (adjusted mean difference vs placebo, -0.55 [95% CI, -1.45 to 0.36]). Treatment-emergent adverse events occurred in between 55.4% and 69.7% of participants in the idalopirdine groups vs between 56.7% and 61.4% of participants in the placebo groups. Conclusions and Relevance: In patients with mild to moderate AD, the use of idalopirdine compared with placebo did not improve cognition over 24 weeks of treatment. These findings do not support the use of idalopirdine for the treatment of AD. Trial Registration: clinicaltrials.gov Identifiers: NCT01955161, NCT02006641, and NCT02006654.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Benzilaminas/uso terapêutico
Inibidores da Colinesterase/uso terapêutico
Indóis/uso terapêutico
Antagonistas da Serotonina/uso terapêutico
[Mh] Termos MeSH secundário: Acidentes por Quedas
Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/psicologia
Benzilaminas/administração & dosagem
Benzilaminas/efeitos adversos
Inibidores da Colinesterase/efeitos adversos
Cognição/efeitos dos fármacos
Relação Dose-Resposta a Droga
Método Duplo-Cego
Quimioterapia Combinada
Feminino
Galantamina/uso terapêutico
Seres Humanos
Indanos/uso terapêutico
Indóis/administração & dosagem
Indóis/efeitos adversos
Masculino
Meia-Idade
Piperidinas/uso terapêutico
Rivastigmina/uso terapêutico
Antagonistas da Serotonina/administração & dosagem
Antagonistas da Serotonina/efeitos adversos
Falha de Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 ((2-(6-fluoro-1H-indol-3-yl)-ethyl)-(3-(2,2,3,3-tetrafluoropropoxy)benzyl)amine); 0 (Benzylamines); 0 (Cholinesterase Inhibitors); 0 (Indans); 0 (Indoles); 0 (Piperidines); 0 (Serotonin Antagonists); 0D3Q044KCA (Galantamine); 8SSC91326P (donepezil); PKI06M3IW0 (Rivastigmine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180311
[Lr] Data última revisão:
180311
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180111
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.20373


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[PMID]:29268129
[Au] Autor:Cen J; Guo H; Hong C; Lv J; Yang Y; Wang T; Fang D; Luo W; Wang C
[Ad] Endereço:Key Laboratory of Natural Medicine and Immuno-Engineering, Henan University, Kaifeng 475004, China.
[Ti] Título:Development of tacrine-bifendate conjugates with improved cholinesterase inhibitory and pro-cognitive efficacy and reduced hepatotoxicity.
[So] Source:Eur J Med Chem;144:128-136, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A novel series of tacrine-bifendate (THA-DDB) conjugates (7a-e) were synthesized and evaluated as potential anti-Alzheimer's agents. These compounds showed potent cholinesterase and self-induced ß-amyloid (Aß) aggregation inhibitory activities. A Lineweaver-Burk plot and molecular modeling study showed that these compounds can target both catalytic active site (CAS) and peripheral anionic site (PAS) of acetylcholinesterase (AChE). The cytotoxicity of the conjugate 7d against PC12 and HepG2 cells and hepatotoxicity against human hepatocyte cell line (HL-7702) were found to be considerably less compared to THA. Moreover, treatment with 7d did not exhibit significant hepatotoxicity in mice. Finally, in vivo studies confirmed that 7d significantly ameliorates the cognitive performances of scopolamine-treated ICR mice. Therefore, 7d has high potential for the treatment of Alzheimer's disease and warrants further investigation.
[Mh] Termos MeSH primário: Compostos de Bifenilo/química
Compostos de Bifenilo/farmacologia
Inibidores da Colinesterase/química
Inibidores da Colinesterase/farmacologia
Cognição/efeitos dos fármacos
Tacrina/análogos & derivados
Tacrina/farmacologia
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/patologia
Animais
Compostos de Bifenilo/toxicidade
Linhagem Celular
Doença Hepática Induzida por Substâncias e Drogas/etiologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
Inibidores da Colinesterase/toxicidade
Colinesterases/metabolismo
Desenho de Drogas
Células Hep G2
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/patologia
Masculino
Camundongos Endogâmicos ICR
Células PC12
Ratos
Tacrina/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biphenyl Compounds); 0 (Cholinesterase Inhibitors); 0G32E321W1 (bifendate); 4VX7YNB537 (Tacrine); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Cholinesterases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29107146
[Au] Autor:Jang JY; Rhim H; Kang S
[Ad] Endereço:Division of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
[Ti] Título:NABi, a novel ß-sheet breaker, inhibits Aß aggregation and neuronal toxicity: Therapeutic implications for Alzheimer's disease.
[So] Source:Biochim Biophys Acta;1862(1):71-80, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Amyloid beta (Aß) aggregates are an important therapeutic target for Alzheimer's disease (AD), a fatal neurodegenerative disease. To date, AD still remains a big challenge due to no effective treatments. Based on the property that Aß aggregates have the cross-ß-structure, a common structural feature in amyloids, we systemically designed the Aß-aggregation inhibitor that maintains Aß-interacting ability but removes toxic part from SOD1 (superoxide dismutase 1)-G93A. We identified NABi (Natural Aß Binder and Aß-aggregation inhibitor) composed of ß2-3 strands, a novel breaker of Aß aggregation, which does not self-aggregate and has no cytotoxicity at all. The NABi blocks Aß-fibril formation in vitro and in vivo and prevents neuronal cell death, a hallmark of AD pathogenesis. Such anti-amyloidogenic properties can provide novel strategies for treating AD. Furthermore, our study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic ß-sheet proteins other than Aß.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/antagonistas & inibidores
Neurônios/metabolismo
Agregação Patológica de Proteínas/tratamento farmacológico
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides/metabolismo
Animais
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Neurônios/patologia
Agregação Patológica de Proteínas/metabolismo
Agregação Patológica de Proteínas/patologia
Estrutura Secundária de Proteína
Superóxido Dismutase/antagonistas & inibidores
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); EC 1.15.1.1 (SOD1 G93A protein); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171107
[St] Status:MEDLINE


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[PMID]:27776566
[Au] Autor:Khusaifan SJ; El Keshky ME
[Ad] Endereço:Department of Psychology,Faculty of Arts and Humanities,King Abdulaziz University,Jeddah,Saudi Arabia.
[Ti] Título:Social support as a mediator variable of the relationship between depression and life satisfaction in a sample of Saudi caregivers of patients with Alzheimer's disease.
[So] Source:Int Psychogeriatr;29(2):239-248, 2017 02.
[Is] ISSN:1741-203X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Caring for someone with Alzheimer's disease (AD) is very challenging. Social support may play a crucial role in helping caregivers to adapt better to their caregiving role. The aim of this study is to explore the role of social support as a moderator variable of the relationship between depression and life satisfaction in caregivers for patients with AD in Saudi Arabia. METHODS: In this cross-sectional study, 122 caregivers for patients with AD completed questionnaires assessing informal social support, depressive symptoms, and general life satisfaction. RESULTS: The demographic characteristics showed that 79% (n = 96) of caregivers were females and between the ages of 20 and 50. Higher levels of social support positively correlated with reported higher levels of life satisfaction (r = 0.483, p < 0.001). Depression was negatively correlated with social support (r = -0.418, p < 0.001) and life satisfaction scores (r = -0.553, p = < 0.001). Social support was found to be a partial mediator variable, mediating approximately 23.05% of the total effect of depression on life satisfaction (Sobel = -3.065, p = 0.002). CONCLUSION: Informal social support can act as a mediator variable in the relationship of depression and life satisfaction in caregivers of AD patients. Improving the informal social support networks may help in coping with caregiving burden and better quality of life.
[Mh] Termos MeSH primário: Doença de Alzheimer/enfermagem
Cuidadores/psicologia
Depressão/psicologia
Satisfação Pessoal
Apoio Social
[Mh] Termos MeSH secundário: Adaptação Psicológica
Adulto
Estudos Transversais
Feminino
Seres Humanos
Masculino
Meia-Idade
Qualidade de Vida/psicologia
Análise de Regressão
Arábia Saudita
Inquéritos e Questionários
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1017/S1041610216001824


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[PMID]:29262769
[Au] Autor:Ray S; Hossain SMM; Khatun L; Mukhopadhyay A
[Ad] Endereço:Department of Computer Science and Engineering, Aliah University, Kolkata, 700156, West Bengal, India.
[Ti] Título:A comprehensive analysis on preservation patterns of gene co-expression networks during Alzheimer's disease progression.
[So] Source:BMC Bioinformatics;18(1):579, 2017 Dec 20.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alzheimer's disease (AD) is a chronic neuro-degenerative disruption of the brain which involves in large scale transcriptomic variation. The disease does not impact every regions of the brain at the same time, instead it progresses slowly involving somewhat sequential interaction with different regions. Analysis of the expression patterns of the genes in different regions of the brain influenced in AD surely contribute for a enhanced comprehension of AD pathogenesis and shed light on the early characterization of the disease. RESULTS: Here, we have proposed a framework to identify perturbation and preservation characteristics of gene expression patterns across six distinct regions of the brain ("EC", "HIP", "PC", "MTG", "SFG", and "VCX") affected in AD. Co-expression modules were discovered considering a couple of regions at once. These are then analyzed to know the preservation and perturbation characteristics. Different module preservation statistics and a rank aggregation mechanism have been adopted to detect the changes of expression patterns across brain regions. Gene ontology (GO) and pathway based analysis were also carried out to know the biological meaning of preserved and perturbed modules. CONCLUSIONS: In this article, we have extensively studied the preservation patterns of co-expressed modules in six distinct brain regions affected in AD. Some modules are emerged as the most preserved while some others are detected as perturbed between a pair of brain regions. Further investigation on the topological properties of preserved and non-preserved modules reveals a substantial association amongst "betweenness centrality" and "degree" of the involved genes. Our findings may render a deeper realization of the preservation characteristics of gene expression patterns in discrete brain regions affected by AD.
[Mh] Termos MeSH primário: Doença de Alzheimer
Biologia Computacional/métodos
Perfilação da Expressão Gênica/métodos
Redes Reguladoras de Genes/genética
Transcriptoma
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Doença de Alzheimer/metabolismo
Doença de Alzheimer/fisiopatologia
Encéfalo/metabolismo
Progressão da Doença
Seres Humanos
Transcriptoma/genética
Transcriptoma/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1946-8


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[PMID]:28452906
[Au] Autor:Hsu CW; Lee Y; Lee CY; Lin PY
[Ad] Endereço:Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
[Ti] Título:Reversible Pisa Syndrome Induced by Rivastigmine in a Patient With Early-Onset Alzheimer Disease.
[So] Source:Clin Neuropharmacol;40(3):147-148, 2017 May/Jun.
[Is] ISSN:1537-162X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pisa syndrome (PS) is a state of dystonic muscle contraction with a marked truncal deviation to one side. It is an uncommon adverse effect of antipsychotic drugs, but is rarely reported in patients receiving acetylcholinesterase inhibitors, especially rivastigmine. We present a 57-year-old female patient with Alzheimer disease who began to develop symptoms of dementia at the age of 51 years. She was observed to have symptoms of PS after continuous use of rivastigmine (9 mg/d) for nearly 2 years. The PS symptoms improved after the dose of rivastigmine was reduced but recurred when the dose was added back to 9 mg/d. Finally, after we decreased the dose to 4.5 mg/d, her PS symptoms were remitted. This report reminds us that clinicians need to be cautious about the risk of PS when prescribing rivastigmine in a patient with early-onset Alzheimer disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Inibidores da Colinesterase/efeitos adversos
Fármacos Neuroprotetores/efeitos adversos
Síndromes Neurotóxicas/terapia
Rivastigmina/efeitos adversos
[Mh] Termos MeSH secundário: Inibidores da Colinesterase/administração & dosagem
Inibidores da Colinesterase/uso terapêutico
Relação Dose-Resposta a Droga
Monitoramento de Medicamentos
Distúrbios Distônicos/etiologia
Distúrbios Distônicos/prevenção & controle
Feminino
Seres Humanos
Meia-Idade
Neuroimagem
Fármacos Neuroprotetores/administração & dosagem
Fármacos Neuroprotetores/uso terapêutico
Síndromes Neurotóxicas/diagnóstico por imagem
Síndromes Neurotóxicas/fisiopatologia
Rivastigmina/administração & dosagem
Rivastigmina/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (Neuroprotective Agents); PKI06M3IW0 (Rivastigmine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1097/WNF.0000000000000215


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[PMID]:27770636
[Au] Autor:Mez J; Chung J; Jun G; Kriegel J; Bourlas AP; Sherva R; Logue MW; Barnes LL; Bennett DA; Buxbaum JD; Byrd GS; Crane PK; Ertekin-Taner N; Evans D; Fallin MD; Foroud T; Goate A; Graff-Radford NR; Hall KS; Kamboh MI; Kukull WA; Larson EB; Manly JJ; Haines JL; Mayeux R; Pericak-Vance MA; Schellenberg GD; Lunetta KL; Farrer LA; Alzheimer's Disease Genetics Consortium
[Ad] Endereço:Department of Neurology, Boston University School of Medicine, Boston, MA, USA; Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA. Electronic address: jessemez@bu.edu.
[Ti] Título:Two novel loci, COBL and SLC10A2, for Alzheimer's disease in African Americans.
[So] Source:Alzheimers Dement;13(2):119-129, 2017 Feb.
[Is] ISSN:1552-5279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: African Americans' (AAs) late-onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power. METHODS: We conducted a genome-wide association study (GWAS) in AAs employing informed conditioning in 1825 LOAD cases and 3784 cognitively normal controls. We derived a posterior liability conditioned on age, sex, diabetes status, current smoking status, educational attainment, and affection status, with parameters informed by external prevalence information. We assessed association between the posterior liability and a genome-wide set of single-nucleotide polymorphisms (SNPs), controlling for APOE and ABCA7, identified previously in a LOAD GWAS of AAs. RESULTS: Two SNPs at novel loci, rs112404845 (P = 3.8 × 10 ), upstream of COBL, and rs16961023 (P = 4.6 × 10 ), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability. DISCUSSION: An informed conditioning approach can detect LOAD genetic associations in AAs not identified by traditional GWAS.
[Mh] Termos MeSH primário: Afroamericanos/genética
Doença de Alzheimer/etnologia
Doença de Alzheimer/genética
Loci Gênicos
Proteínas dos Microfilamentos/genética
Transportadores de Ânions Orgânicos Dependentes de Sódio/genética
Polimorfismo de Nucleotídeo Único
Simportadores/genética
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/genética
Idoso
Idoso de 80 Anos ou mais
Apolipoproteínas E/genética
Complicações do Diabetes/etnologia
Complicações do Diabetes/genética
Escolaridade
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Prevalência
Fumar/etnologia
Fumar/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA7 protein, human); 0 (ATP-Binding Cassette Transporters); 0 (Apolipoproteins E); 0 (Cobl protein, human); 0 (Microfilament Proteins); 0 (Organic Anion Transporters, Sodium-Dependent); 0 (Symporters); 145420-23-1 (sodium-bile acid cotransporter)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status: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


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[PMID]:29335400
[Au] Autor:Zhu Z; Zheng Z; Zhang F; Wu Y; Trzaskowski M; Maier R; Robinson MR; McGrath JJ; Visscher PM; Wray NR; Yang J
[Ad] Endereço:Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, 4072, Australia.
[Ti] Título:Causal associations between risk factors and common diseases inferred from GWAS summary data.
[So] Source:Nat Commun;9(1):224, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. It often remains unclear whether the risk factors are cause or consequence of disease, or whether the associations are the result of confounding. We develop and apply a method (called GSMR) that performs a multi-SNP Mendelian randomization analysis using summary-level data from genome-wide association studies to test the causal associations of BMI, waist-to-hip ratio, serum cholesterols, blood pressures, height, and years of schooling (EduYears) with common diseases (sample sizes of up to 405,072). We identify a number of causal associations including a protective effect of LDL-cholesterol against type-2 diabetes (T2D) that might explain the side effects of statins on T2D, a protective effect of EduYears against Alzheimer's disease, and bidirectional associations with opposite effects (e.g., higher BMI increases the risk of T2D but the effect of T2D on BMI is negative).
[Mh] Termos MeSH primário: Índice de Massa Corporal
Colesterol/sangue
Doença/genética
Estudo de Associação Genômica Ampla/métodos
[Mh] Termos MeSH secundário: Doença de Alzheimer/sangue
Doença de Alzheimer/genética
LDL-Colesterol/sangue
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/genética
Doença/etiologia
Seres Humanos
Análise da Randomização Mendeliana
Polimorfismo de Nucleotídeo Único
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cholesterol, LDL); 97C5T2UQ7J (Cholesterol)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02317-2


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[PMID]:29353726
[Au] Autor:Czarnecka K; Chufarova N; Halczuk K; Maciejewska K; Girek M; Skibinski R; Jonczyk J; Bajda M; Kabzinski J; Majsterek I; Szymanski P
[Ad] Endereço:Department of Pharmaceutical Chemistry, Drug Analyses and Radiopharmacy, Faculty of Pharmacy, Medical University of Lodz, Muszynskiego 1, 90-151 Lodz, Poland. Electronic address: kamila.czarnecka@umed.lodz.pl.
[Ti] Título:Tetrahydroacridine derivatives with dichloronicotinic acid moiety as attractive, multipotent agents for Alzheimer's disease treatment.
[So] Source:Eur J Med Chem;145:760-769, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A novel series of 9-amino-1,2,3,4-tetrahydroacridine and 5,6-dichloronicotinic acid moiety were conjugated with different linkers. Afterwards new derivatives were evaluated as potential multifunctional acetylcholinesterase inhibitors (AChEIs), anti-Alzheimer's disease (AD) drug candidates. All the compounds were synthesized and tested for capacity for the inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) enzymes. Specifically, the most promising derivative 3b (IC = 1.02 nM) had higher inhibitory potency compared to the reference drug, tacrine. Consequently, kinetic studies of 3b compound showed a mixed-type inhibition of both AChE and BuChE. Afterwards the best potent AChE inhibitor has been examined on amyloid ß (Aß) self-induced aggregation. Furthermore, 3b compound was tested in various concentrations and had moderate activity against Aß aggregation. Inhibition of Aß aggregation was 46.63% and 19.41% at 50 µM and 5  µM concentrations, respectively. Moreover, no cytotoxicity was observed for the mentioned concentrations. Therefore, 3b compound is a promising multipotent agent for the treatment of AD.
[Mh] Termos MeSH primário: Acetilcolinesterase/metabolismo
Acridinas/farmacologia
Doença de Alzheimer/tratamento farmacológico
Butirilcolinesterase/metabolismo
Inibidores da Colinesterase/farmacologia
Ácidos Nicotínicos/farmacologia
[Mh] Termos MeSH secundário: Acridinas/química
Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/antagonistas & inibidores
Peptídeos beta-Amiloides/metabolismo
Animais
Inibidores da Colinesterase/síntese química
Inibidores da Colinesterase/química
Relação Dose-Resposta a Droga
Electrophorus
Cavalos
Seres Humanos
Modelos Moleculares
Estrutura Molecular
Ácidos Nicotínicos/química
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5,6-dichloronicotinic acid); 0 (Acridines); 0 (Amyloid beta-Peptides); 0 (Cholinesterase Inhibitors); 0 (Nicotinic Acids); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE



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