Current research therapeutic strategies for Alzheimer's disease treatment

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 hypo...

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Autores: Folch, 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
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2016
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/105536
Acceso en línea:https://hdl.handle.net/2445/105536
Access Level:acceso abierto
Palabra clave:Malaltia d&apos
Alzheimer
Terapèutica
Alzheimer&apos
s disease
Therapeutics
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spelling Current research therapeutic strategies for Alzheimer's disease treatmentFolch, JaumePetrov, DmitryEttcheto Arriola, MirenAbad, SoniaSánchez-López, E. (Elena)García López, María LuisaOlloquequi, JordiBeas Zárate, CarlosAuladell i Costa, M. CarmeCamins Espuny, AntoniMalaltia d&aposAlzheimerTerapèuticaAlzheimer&aposs diseaseTherapeuticsAlzheimer'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.Hindawi2017201720162017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion16 p.application/pdfhttps://hdl.handle.net/2445/105536Articles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReproducció del document publicat a: https://doi.org/10.1155/2016/8501693Neural Plasticity, 2016, vol. 2016, p. 1-15https://doi.org/10.1155/2016/8501693cc-by (c) Folch López, Jaume et al., 2016http://creativecommons.org/licenses/by/3.0/esinfo:eu-repo/semantics/openAccessoai:recercat.cat:2445/1055362026-05-29T05:05:01Z
dc.title.none.fl_str_mv Current research therapeutic strategies for Alzheimer's disease treatment
title Current research therapeutic strategies for Alzheimer's disease treatment
spellingShingle Current research therapeutic strategies for Alzheimer's disease treatment
Folch, Jaume
Malaltia d&apos
Alzheimer
Terapèutica
Alzheimer&apos
s disease
Therapeutics
title_short Current research therapeutic strategies for Alzheimer's disease treatment
title_full Current research therapeutic strategies for Alzheimer's disease treatment
title_fullStr Current research therapeutic strategies for Alzheimer's disease treatment
title_full_unstemmed Current research therapeutic strategies for Alzheimer's disease treatment
title_sort Current research therapeutic strategies for Alzheimer's disease treatment
dc.creator.none.fl_str_mv Folch, 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
author Folch, Jaume
author_facet Folch, 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
author_role author
author2 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
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Malaltia d&apos
Alzheimer
Terapèutica
Alzheimer&apos
s disease
Therapeutics
topic Malaltia d&apos
Alzheimer
Terapèutica
Alzheimer&apos
s disease
Therapeutics
description 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.
publishDate 2016
dc.date.none.fl_str_mv 2016
2017
2017
2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/105536
url https://hdl.handle.net/2445/105536
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.1155/2016/8501693
Neural Plasticity, 2016, vol. 2016, p. 1-15
https://doi.org/10.1155/2016/8501693
dc.rights.none.fl_str_mv cc-by (c) Folch López, Jaume et al., 2016
http://creativecommons.org/licenses/by/3.0/es
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by (c) Folch López, Jaume et al., 2016
http://creativecommons.org/licenses/by/3.0/es
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 16 p.
application/pdf
dc.publisher.none.fl_str_mv Hindawi
publisher.none.fl_str_mv Hindawi
dc.source.none.fl_str_mv Articles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,811543

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