Molecular links between early energy metabolism alterations and Alzheimer´s disease
Recent studies suggest that the neurobiology of Alzheimer's disease (AD) pathology could not be explained solely by an increase in beta-amyloid levels. In fact, success with potential therapeutic drugs that inhibit the generation of beta amyloid has been low. Therefore, due to therapeutic failu...
| Autores: | , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión aceptada para publicación |
| Fecha de publicación: | 2016 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/138560 |
| Acceso en línea: | https://hdl.handle.net/2445/138560 |
| Access Level: | acceso abierto |
| Palabra clave: | Malaltia d'Alzheimer Metabolisme energètic Alzheimer's disease Energy metabolism |
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Molecular links between early energy metabolism alterations and Alzheimer´s diseasePedros, IgnacioPatraca, IvanMartínez, NaroaPetrov, DmitrySureda, Francesc X.Auladell i Costa, M. CarmeBeas Zárate, CarlosFolch, JaumeMalaltia d'AlzheimerMetabolisme energèticAlzheimer's diseaseEnergy metabolismRecent studies suggest that the neurobiology of Alzheimer's disease (AD) pathology could not be explained solely by an increase in beta-amyloid levels. In fact, success with potential therapeutic drugs that inhibit the generation of beta amyloid has been low. Therefore, due to therapeutic failure in recent years, the scientists are looking for alternative hypotheses to explain the causes of the disease and the cognitive loss. Accordingly, alternative hypothesis propose a link between AD and peripheral metabolic alteration. Then, we review in depth changes related to insulin signalling and energy metabolism in the context of the APPSwe/PS1dE9 (APP/PS1) mice model of AD. We show an integrated view of the changes that occur in the early stages of the amyloidogenic process in the APP/PS1 double transgenic mice model. These early changes affect several key metabolic processes related to glucose uptake and insulin signalling, cellular energy homeostasis, mitochondrial biogenesis and increased Tau phosphorylation by kinase molecules like mTOR and Cdk5.Frontiers in Bioscience2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/2445/138560Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésVersió postprint del document publicat a: https://doi.org/10.2741/4372Frontiers in Bioscience-Landmark Edition, 2016, vol. 1, num. 21, p. 8-19https://doi.org/10.2741/4372(c) Frontiers in Bioscience, 2016info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1385602026-05-27T06:46:51Z |
| dc.title.none.fl_str_mv |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| title |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| spellingShingle |
Molecular links between early energy metabolism alterations and Alzheimer´s disease Pedros, Ignacio Malaltia d'Alzheimer Metabolisme energètic Alzheimer's disease Energy metabolism |
| title_short |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| title_full |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| title_fullStr |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| title_full_unstemmed |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| title_sort |
Molecular links between early energy metabolism alterations and Alzheimer´s disease |
| dc.creator.none.fl_str_mv |
Pedros, Ignacio Patraca, Ivan Martínez, Naroa Petrov, Dmitry Sureda, Francesc X. Auladell i Costa, M. Carme Beas Zárate, Carlos Folch, Jaume |
| author |
Pedros, Ignacio |
| author_facet |
Pedros, Ignacio Patraca, Ivan Martínez, Naroa Petrov, Dmitry Sureda, Francesc X. Auladell i Costa, M. Carme Beas Zárate, Carlos Folch, Jaume |
| author_role |
author |
| author2 |
Patraca, Ivan Martínez, Naroa Petrov, Dmitry Sureda, Francesc X. Auladell i Costa, M. Carme Beas Zárate, Carlos Folch, Jaume |
| author2_role |
author author author author author author author |
| dc.subject.none.fl_str_mv |
Malaltia d'Alzheimer Metabolisme energètic Alzheimer's disease Energy metabolism |
| topic |
Malaltia d'Alzheimer Metabolisme energètic Alzheimer's disease Energy metabolism |
| description |
Recent studies suggest that the neurobiology of Alzheimer's disease (AD) pathology could not be explained solely by an increase in beta-amyloid levels. In fact, success with potential therapeutic drugs that inhibit the generation of beta amyloid has been low. Therefore, due to therapeutic failure in recent years, the scientists are looking for alternative hypotheses to explain the causes of the disease and the cognitive loss. Accordingly, alternative hypothesis propose a link between AD and peripheral metabolic alteration. Then, we review in depth changes related to insulin signalling and energy metabolism in the context of the APPSwe/PS1dE9 (APP/PS1) mice model of AD. We show an integrated view of the changes that occur in the early stages of the amyloidogenic process in the APP/PS1 double transgenic mice model. These early changes affect several key metabolic processes related to glucose uptake and insulin signalling, cellular energy homeostasis, mitochondrial biogenesis and increased Tau phosphorylation by kinase molecules like mTOR and Cdk5. |
| publishDate |
2016 |
| dc.date.none.fl_str_mv |
2016 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/acceptedVersion |
| format |
article |
| status_str |
acceptedVersion |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/2445/138560 |
| url |
https://hdl.handle.net/2445/138560 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Versió postprint del document publicat a: https://doi.org/10.2741/4372 Frontiers in Bioscience-Landmark Edition, 2016, vol. 1, num. 21, p. 8-19 https://doi.org/10.2741/4372 |
| dc.rights.none.fl_str_mv |
(c) Frontiers in Bioscience, 2016 info:eu-repo/semantics/openAccess |
| rights_invalid_str_mv |
(c) Frontiers in Bioscience, 2016 |
| eu_rights_str_mv |
openAccess |
| dc.format.none.fl_str_mv |
application/pdf |
| dc.publisher.none.fl_str_mv |
Frontiers in Bioscience |
| publisher.none.fl_str_mv |
Frontiers in Bioscience |
| dc.source.none.fl_str_mv |
Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia) reponame:Dipòsit Digital de la UB instname:Universidad de Barcelona |
| instname_str |
Universidad de Barcelona |
| reponame_str |
Dipòsit Digital de la UB |
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Dipòsit Digital de la UB |
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|
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1869417199227109376 |
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15.301603 |