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Por favor, use este identificador para citar o enlazar este ítem: http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17125
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dc.rights.licensehttp://creativecommons.org/licenses/by-nc/4.0es_MX
dc.creatorISABEL ARRIETA CRUZes_MX
dc.creatorROGER GUTIERREZ JUAREZes_MX
dc.date2016-
dc.date.accessioned2018-12-19T19:18:10Z-
dc.date.available2018-12-19T19:18:10Z-
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17125-
dc.descriptionAbstract: Alzheimer´s disease is a chronic neurodegenerative disorder affecting millions of people worldwide, characterized by a progressive decline in cognitive functions. Factors involved in the pathogenesis of Alzheimer´s disease include metabolic alterations such as insulin resistance and hyperglycemia, both of which are also hallmarks of type-2 diabetes mellitus. The accumulation of β-amyloid peptides in the brain of Alzheimer´s patients is responsible in part for the neurotoxicity underlying the loss of synaptic plasticity that triggers a cascade of events leading to cell death. A large number of studies revealed the key role of the hippocampus and cerebral cortex in the memory and learning deficits of Alzheimer´s disease. Although ample evidence suggests a link between altered insulin action, the dysregulation of glucose metabolism, and β-amyloid accumulation in animal models and humans with Alzheimer´s, no supporting evidence was available. In this article, we review the potential toxic effects of β-amyloid in the hypothalamus, a brain center involved in the control of insulin action and glucose metabolism. Furthermore, we discuss our recent studies unraveling a novel neurotoxic action of β-amyloid that perturbs hypothalamic glucoregulation, leading to increased hepatic glucose production and hyperglycemia. These findings provide evidence for a link between β-amyloid toxicity and altered glucose metabolism.es_MX
dc.descriptionConclusions: In conclusion, studies on the molecular and cellular mechanisms involved in the pathophysiology of AD and its relationship with insulin and glucose metabolism support the idea that the metabolic alterations of DM2 are strongly associated to the development of AD. Importantly, our recent studies in rodents provided a piece of evidence supporting the novel concept that AB toxic action in the hypothalamus causes a dysregulation of glucose metabolism directly linking altered insulin action with AD. Further studies are required to better understand the details of this relationship and its causal role, if any, in the onset and progression of AD.es_MX
dc.formatAdobe PDFes_MX
dc.languagespaes_MX
dc.publisherInstituto Nacional de Ciencias Medicas y Nutrición Salvador Zubiránes_MX
dc.relationhttp://clinicalandtranslationalinvestigation.com/abstract.php?id=79es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceRevista de Investigación Clínica (0034-8376) vol. 68 (2016)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectCiencias de la vidaes_MX
dc.subjectBioquímicaes_MX
dc.subjectEnfermedades del sistema nerviosoes_MX
dc.subjectEnfermedades neurodegenerativases_MX
dc.subjectTauopatíases_MX
dc.subjectAlzheimer, Enfermedad dees_MX
dc.subjectEnfermedades metabólicases_MX
dc.subjectTrastornos del metabolismo de la glucosaes_MX
dc.subjectDiabetes mellituses_MX
dc.subjectResistencia a la insulinaes_MX
dc.subjectBiochemistryes_MX
dc.subjectNervous system diseaseses_MX
dc.subjectNeurodegenerative diseaseses_MX
dc.subjectTauopathieses_MX
dc.subjectAlzheimer diseasees_MX
dc.subjectMetabolic diseaseses_MX
dc.subjectGlucose metabolism disorderses_MX
dc.subjectDiabetes mellituses_MX
dc.subjectInsuline resistancees_MX
dc.titleThe role of insulin resistance and glucose metabolism dysregulation in the development of Alzheimer's diseasees_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.idAICI730724MDFRRS06es_MX
dc.creator.idGUJR600202HOCTRG04es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
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