Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/9289
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dc.contributor.authorMartino Adami, Pamela V.es
dc.contributor.authorGaleano, Pabloes
dc.contributor.authorWallinger, Marina L.es
dc.contributor.authorQuijano, Celiaes
dc.contributor.authorRabossi, Alejandroes
dc.contributor.authorPagano, Eleonora Samantaes
dc.contributor.authorOlivar, Natividades
dc.contributor.authorReyes Toso, Carlos F.es
dc.contributor.authorCardinali, Daniel Pedroes
dc.contributor.authorBrusco, Luis I.es
dc.contributor.authorDo Carmo, Soniaes
dc.contributor.authorRadi, Rafaeles
dc.contributor.authorGevorkian, Goares
dc.contributor.authorCastaño, Eduardo M.es
dc.contributor.authorCuello, A. Claudioes
dc.contributor.authorMorelli, Lauraes
dc.date.accessioned2019-12-17T00:21:35Z-
dc.date.available2019-12-17T00:21:35Z-
dc.date.issued2016-
dc.identifier.citationMartino Adami, P. V., et al. Worsening of memory deficit induced by energy-dense diet in a rat model of early-Alzheimer's disease is associated to neurotoxic Aβ species and independent of neuroinflammation [en línea]. Biochimica et Biophysica Acta - Molecular Basis of Disease. 2016, 1863(3). doi: 10.1016/j.bbadis.2016.12.014. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/9289es
dc.identifier.issn0925-4439 (en línea)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/9289-
dc.description.abstractAbstract: Diet is a modifiable risk factor for Alzheimer's disease (AD), but the mechanisms linking alterations in peripheral metabolism and cognition remain unclear. Since it is especially difficult to study long-term effects of high-energy diet in individuals at risk for AD, we addressed this question by using the McGill-R-Thy1-APP transgenic rat model (Tg(+/-)) that mimics presymptomatic AD. Wild-type and Tg(+/-) rats were exposed during 6months to a standard diet or a Western diet (WD), high in saturated fat and sugar. Results from peripheral and hippocampal biochemical analysis and in situ respirometry showed that WD induced a metabolic syndrome and decreased presynaptic bioenergetic parameters without alterations in hippocampal insulin signaling or lipid composition. Cognitive tests, ELISA multiplex, Western blot, immunohistochemistry and RT-qPCR indicated that WD worsened cognition in Tg(+/-) rats, increased hippocampal levels of monomeric Aβ isoforms and oligomeric species, promoted deposits of N-Terminal pyroglutamate-Aβ (AβN3(pE)) in CA1 pyramidal neurons and interneurons, decreased transcript levels of genes involved in neuroprotective pathways such as Sirtuin-1 and increased nitrated proteins. Our results support the concept that in the presence of early Aβ pathology, diet-induced metabolic dysfunctions may contribute as a "second hit" to impair cognition. Noteworthy, such effect is not mediated by higher microglia activation or disruption of blood brain barrier. However, it may be attributed to increased amyloidogenic processing of amyloid precursor protein, generation of AβN3(pE) and dysregulation of pathways governed by Sirtuin-1. This evidence reinforces the implementation of prophylactic interventions in individuals at risk for AD.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherElsevieres
dc.rightsAcceso abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceBiochimica et Biophysica Acta - Molecular Basis of Disease. 2016, 1863(3)es
dc.subjectENFERMEDAD DE ALZHEIMERes
dc.subjectDIETAes
dc.subjectENFERMEDADES METABOLICASes
dc.subjectHIPERTENSIONes
dc.subjectMEMORIAes
dc.subjectENFERMEDADES NEURODEGENERATIVASes
dc.titleWorsening of memory deficit induced by energy-dense diet in a rat model of early-Alzheimer's disease is associated to neurotoxic Aβ species and independent of neuroinflammationes
dc.typeArtículoes
dc.identifier.doi10.1016/j.bbadis.2016.12.014-
dc.identifier.pmid28039031-
uca.disciplinaMEDICINAes
uca.issnrd1es
uca.affiliationFil: Martino Adami, Pamela V. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Martino Adami, Pamela V. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentinaes
uca.affiliationFil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Galeano, Pablo. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentinaes
uca.affiliationFil: Galeano, Pablo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentinaes
uca.affiliationFil: Wallinger, Marina L. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentinaes
uca.affiliationFil: Quijano, Celia. Universidad de la República. Facultad de Medicina. Department of Biochemistry Center for Free Radical and Biomedical Research; Uruguayes
uca.affiliationFil: Rabossi, Alejandro. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Biochemistry and Molecular Biology of Development; Argentinaes
uca.affiliationFil: Rabossi, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Pagano, Eleonora Samanta. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentinaes
uca.affiliationFil: Olivar, Natividad. Universidad de Buenos Aires. Facultad de Medicina. Centro de Neuropsiquiatría y Neurología de la Conducta. Unidad Académica II. Departamento de Ciencias Fisiológicas; Argentinaes
uca.affiliationFil: Reyes Toso, Carlos F. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentinaes
uca.affiliationFil: Cardinali, Daniel Pedro. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas. Unidad Académica II; Argentinaes
uca.affiliationFil: Brusco, Luis I. Universidad de Buenos Aires. Facultad de Medicina. Centro de Neuropsiquiatría y Neurología de la Conducta. Unidad Académica II. Departamento de Ciencias Fisiológicas; Argentinaes
uca.affiliationFil: Do Carmo, Sonia. McGill University. Department of Pharmacology and Therapeutics; Canadáes
uca.affiliationFil: Radi, Rafael. Universidad de la República. Facultad de Medicina. Department of Biochemistry Center for Free Radical and Biomedical Research; Uruguayes
uca.affiliationFil: Gevorkian, Goar. Universidad Nacional Autónoma de México. Instituto de Investigaciones Biomédicas; Méxicoes
uca.affiliationFil: Castaño, Eduardo M. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentinaes
uca.affiliationFil: Castaño, Eduardo M. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Cuello, A. Claudio. McGill University. Department of Pharmacology and Therapeutics; Canadáes
uca.affiliationFil: Laura Morelli. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires. Laboratory of Amyloidosis and Neurodegeneration; Argentinaes
uca.affiliationFil: Laura Morelli. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.versionpublishedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Psiconeuroendocrinoinmunología-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.orcid0000-0002-0813-9088-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
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