Autor segons l'article: Jaume Folch; Dmitry Petrov; Miren Ettcheto; Sonia Abad; Elena Sánchez-López; M. Luisa García; Jordi Olloquequi; Carlos Beas-Zarate; Carme Auladell; Antoni Camins
Departament: Bioquímica i Biotecnologia
Autor/s 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
Paraules clau: Amyloid beta protein
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 (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.
Grup de recerca: Farmacobiologia Cel.lular
Àrees temàtiques: Bioquímica i biotecnologia Bioquímica y tecnología Biochemistry and technology
Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
ISSN: 2090-5904
Data d'alta del registre: 2016-07-27
Volum de revista: 2016
Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
Enllaç font original: https://www.hindawi.com/journals/np/2016/8501693/
URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
DOI de l'article: 10.1155/2016/8501693
Entitat: Universitat Rovira i Virgili
Any de publicació de la revista: 2016
Pàgina inicial: Art.num. 8501693
Tipus de publicació: Article Artículo Article
Repositori URV