Autor según el artículo: Folch J; Petrov D; Ettcheto M; Abad S; Sánchez-López E; García ML; Olloquequi J; Beas-Zarate C; Auladell C; Camins A

Departamento: Bioquímica i Biotecnologia

Autor/es de la URV: Folch Lopez, Jaume

Palabras clave: Selective monoamine-oxidase Mild cognitive impairment Intranasal insulin Gamma-secretase Double-blind Central-nervous-system Avagacestat bms-708163 Amyloid-beta Amyloid beta protein Aggregation inhibitor therapy A-beta-oligomers

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 (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.

Áreas temáticas: 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

Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/

ISSN: 07928483

Direcció de correo del autor: jaume.folch@urv.cat

Identificador del autor: 0000-0002-5051-8858

Fecha de alta del registro: 2023-02-18

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: http://repositori.urv.cat/ca/proteccio-de-dades/

Referencia al articulo segun fuente origial: Neural Plasticity. 2016 (8501693): 8501693-

Referencia de l'ítem segons les normes APA: Folch J; Petrov D; Ettcheto M; Abad S; Sánchez-López E; García ML; Olloquequi J; Beas-Zarate C; Auladell C; Camins A (2016). Current Research Therapeutic Strategies for Alzheimer's Disease Treatment. Neural Plasticity, 2016(8501693), 8501693-. DOI: 10.1155/2016/8501693

DOI del artículo: 10.1155/2016/8501693

Entidad: Universitat Rovira i Virgili

Año de publicación de la revista: 2016

Tipo de publicación: Journal Publications