Autor según el artículo: Jaume Folch; Dmitry Petrov; Miren Ettcheto; Sonia Abad; Elena Sánchez-López; M. Luisa García; Jordi Olloquequi; Carlos Beas-Zarate; Carme Auladell; Antoni Camins
Departamento: Bioquímica i Biotecnologia
Autor/es de la URV: FOLCH LOPEZ, JAUME; Dmitry Petrov; Miren Ettcheto; Sonia Abad; Elena Sánchez-López; M. Luisa García; Jordi Olloquequi; Carlos Beas-Zarate; Carme Auladell; Antoni Camins
Palabras clave: Amyloid beta protein
Resumen: 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 (Aβ) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce Aβ production through the inhibition of β and γ secretase enzymes and (b) to promote dissolution of existing cerebral Aβ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream Aβ signalling, particularly at the synapse. Aβ 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 Aβ 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.
Grupo de investigación: Farmacobiologia Cel.lular
Áreas temáticas: Bioquímica i biotecnologia Bioquímica y tecnología Biochemistry and technology
Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
ISSN: 2090-5904
Fecha de alta del registro: 2016-07-27
Volumen de revista: 2016
Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
Enlace a la fuente original: https://www.hindawi.com/journals/np/2016/8501693/
URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
DOI del artículo: 10.1155/2016/8501693
Entidad: Universitat Rovira i Virgili
Año de publicación de la revista: 2016
Página inicial: Art.num. 8501693
Tipo de publicación: Article Artículo Article
Repositori URV