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Title: Current research therapeutic strategies for Alzheimer's disease treatment
Author: Folch López, Jaume
Petrov, Dmitry
Ettcheto Arriola, Miren
Abad, Sonia
Sánchez-López, E. (Elena)
García López, María Luisa
Olloquequi, Jordi
Beas Zárate, Carlos
Auladell i Costa, M. Carme
Camins Espuny, Antoni
Keywords: Malaltia d'Alzheimer
Alzheimer's disease
Issue Date: 2016
Publisher: Hindawi
Abstract: 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.
Note: Reproducció del document publicat a:
It is part of: Neural Plasticity, 2016, vol. 2016, p. 1-15
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ISSN: 2090-5904
Appears in Collections:Articles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)

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