Autor segons l'article: Folch, Jaume; Petrov, Dmitry; Ettcheto, Miren; Abad, Sonia; Sanchez-Lopez, Elena; Luisa Garcia, M; Olloquequi, Jordi; Beas-Zarate, Carlos; Auladell, Carme; Camins, Antoni
Departament: Bioquímica i Biotecnologia
Autor/s de la URV: Folch Lopez, Jaume
Paraules clau: Thiazoles Synapses Serotonin 6 receptor Selective monoamine-oxidase Saracatinib Receptors, serotonin Receptors, n-methyl-d-aspartate Receptor, metabotropic glutamate 5 Quinazolines Pyridines Prpc proteins Proto-oncogene proteins c-fyn Protein kinase inhibitors Piperidines Neurons Mild cognitive impairment Mice Masitinib Intranasal insulin Humans Grm5 protein, human Gamma-secretase Fyn protein, human Double-blind Disease models, animal Central-nervous-system Brain Benzodioxoles Benzamides Avagacestat bms-708163 Animals Amyloid-beta Amyloid beta-peptides Amyloid beta protein Alzheimer disease Aggregation inhibitor therapy A-beta-oligomers
Resum: Alzheimer's disease (AD) currently presents one of the biggest healthcare issues in the developed countries. There is no effective treatment capable of slowing down disease progression. In recent years the main focus of research on novel pharmacotherapies was based on the amyloidogenic hypothesis of AD, which posits that the beta amyloid (A¿) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce A¿ production through the inhibition of ¿ and ¿ secretase enzymes and (b) to promote dissolution of existing cerebral A¿ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream A¿ signalling, particularly at the synapse. A¿ oligomers may cause aberrant N-methyl-D-aspartate receptor (NMDAR) activation postsynaptically by forming complexes with the cell-surface prion protein (PrPC). PrPC is enriched at the neuronal postsynaptic density, where it interacts with Fyn tyrosine kinase. Fyn activation occurs when A¿ is bound to PrPC-Fyn complex. Fyn causes tyrosine phosphorylation of the NR2B subunit of metabotropic glutamate receptor 5 (mGluR5). Fyn kinase blockers masitinib and saracatinib have proven to be efficacious in treating AD symptoms in experimental mouse models of the disease.
Àrees temàtiques: Transplantation Saúde coletiva Psicología Neurosciences Neurology (clinical) Neurology Medicina veterinaria Medicina ii Medicina i Interdisciplinar Filosofía Farmacia Engenharias iv Educação física Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Ciência da computação
Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
ISSN: 07928483
Adreça de correu electrònic de l'autor: jaume.folch@urv.cat
Identificador de l'autor: 0000-0002-5051-8858
Data d'alta del registre: 2024-10-19
Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
Referència a l'article segons font original: Neural Plasticity. 2016 (8501693): 8501693-
Referència de l'ítem segons les normes APA: Folch, Jaume; Petrov, Dmitry; Ettcheto, Miren; Abad, Sonia; Sanchez-Lopez, Elena; Luisa Garcia, M; Olloquequi, Jordi; Beas-Zarate, Carlos; Auladell, C (2016). Current Research Therapeutic Strategies for Alzheimer's Disease Treatment. Neural Plasticity, 2016(8501693), 8501693-. DOI: 10.1155/2016/8501693
Entitat: Universitat Rovira i Virgili
Any de publicació de la revista: 2016
Tipus de publicació: Journal Publications
Repositori URV