IMR Press / FBL / Volume 21 / Issue 1 / DOI: 10.2741/4372

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Molecular links between early energy metabolism alterations and Alzheimer´s disease

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1 Unitats de Bioquimica i, Facultat de Medicina i Ciencies de la Salut, Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat Rovira i Virgili, C./St. Llorenç 21 43201 Reus (Tarragona), Spain
2 Farmacologia, Facultat de Medicina i Ciencies de la Salut, Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat Rovira i Virgili, C./St. Llorenç 21 43201 Reus (Tarragona), Spain
3 Unitat de Farmacologia i Farmacognosia Facultat de Farmacia, Institut de Biomedicina (IBUB), Centros de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat de Barcelona, Barcelona, Spain
4 Departament de Biologia Cellular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
5 Departamento de Biologia Celular y Molecular, C.U.C.B.A., Universidad de Guadalajara and Division de Neurociencias, Centro de Investigacion Biomedica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. Independencia, Guadalajara, Jalisco 44340, Mexico
Academic Editor:Antoni Camins
Front. Biosci. (Landmark Ed) 2016, 21(1), 8–19; https://doi.org/10.2741/4372
Published: 1 January 2016
(This article belongs to the Special Issue Current advances in epilepsy and neurodegeneration)
Abstract

Recent studies suggest that the neurobiology of Alzheimer’s disease (AD) pathology could not be explained solely by an increase in β-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.

Keywords
APP/PS1
Insulin Receptor
Hippocampus
Alzheimer Disease
Leptin
Prolactin
PGC-1α
mTOR
Cdk5
Review
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