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1-(7-Chloroquinolin-4-yl)-N-(4-Methoxybenzyl)-5-Methyl-1H-1,2, 3-Triazole-4- carboxamide Reduces Aß Formation and Tau Phosphorylation in Cellular Models of Alzheimer's Disease.
Fronza, Mariana G; Sacramento, Manoela; Alves, Diego; Praticò, Domenico; Savegnago, Lucielli.
Afiliação
  • Fronza MG; Neurobiotechnology Research Group (GPN)-Centre for Technology Development CDTec, Federal University of Pelotas (UFPel), Pelotas, RS, Brazil.
  • Sacramento M; Laboratory of Clean Organic Synthesis (LASOL), Center for Chemical, Pharmaceutical and Food Sciences (CCQFA), UFPel, RS, Brazil.
  • Alves D; Laboratory of Clean Organic Synthesis (LASOL), Center for Chemical, Pharmaceutical and Food Sciences (CCQFA), UFPel, RS, Brazil.
  • Praticò D; Alzheimer's Center at Temple-ACT, Temple University, Lewis Katz School of Medicine, Philadelphia, PA, USA. praticod@temple.edu.
  • Savegnago L; Neurobiotechnology Research Group (GPN)-Centre for Technology Development CDTec, Federal University of Pelotas (UFPel), Pelotas, RS, Brazil. lucielli@ufpel.edu.br.
Neurochem Res ; 47(4): 1110-1122, 2022 Apr.
Article em En | MEDLINE | ID: mdl-35165799
1-(7-Chloroquinolin-4-yl)-N-(4-methoxybenzyl)-5-methyl-1H-1,2,3-triazole-4- carboxamide (QTC-4-MeOBnE) is a new multi-target directed ligand (MTDL) rationally designed to have affinity with ß-secretase (BACE), Glycogen Synthase Kinase 3ß (GSK3ß) and acetylcholinesterase, which are considered promising targets on the development of disease-modifying therapies against Alzheimer's Disease (AD). Previously, QTC-4-MeOBnE treatment showed beneficial effects in preclinical AD-like models by influencing in vivo neurogenesis, oxidative and inflammatory pathways. However, the biological effect and mechanism of action exerted by QTC-4-MeOBnE in AD cellular models have not been elucidated yet. Hereby we investigate the acute effect of QTC-4-MeOBnE on neuronal cells overexpressing Amyloid Protein Precursor (APP) or human tau protein, the two main features of the AD pathophysiology. When compared to the control group, QTC-4-MeOBnE treatment prevented amyloid beta (Aß) formation through the downregulation of APP and BACE levels in APPswe-expressing cells. Furthermore, in N2a cells overexpressing human tau, QTC-4-MeOBnE reduced the levels of phosphorylated forms of tau via the modulation of the GSK3ß pathway. Taken together, our findings provide new insights into the mechanism of action exerted by QTC-4-MeOBnE in AD cellular models, and further support its potential as an interesting therapeutic strategy against AD.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Proteínas tau / Doença de Alzheimer Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Neurochem Res Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Proteínas tau / Doença de Alzheimer Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Neurochem Res Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos