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dc.contributor.authorFolch J.
dc.contributor.authorOlloquequi J.
dc.contributor.authorEttcheto M.
dc.contributor.authorBusquets O.
dc.contributor.authorSánchez-López E.
dc.contributor.authorCano A.
dc.contributor.authorEspinosa-Jiménez T.
dc.contributor.authorGarcía M.L.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorCasadesús G.
dc.contributor.authorBulló M.
dc.contributor.authorAuladell C.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:54Z
dc.date.available2020-09-02T22:17:54Z
dc.date.issued2019
dc.identifier10.3389/fnagi.2019.00236
dc.identifier.citation11, , -
dc.identifier.issn16634365
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4492
dc.descriptionNowadays, Alzheimer’s disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its incidence and, for now, there are no effective treatments since current approved medications have only shown short-term symptomatic benefits. Therefore, it is imperative to increase efforts in the search for molecules and non-pharmacological strategies that are capable of slowing or stopping the progress of the disease and, ideally, to reverse it. The amyloid cascade hypothesis based on the fundamental role of amyloid has been the central hypothesis in the last 30 years. However, since amyloid-directed treatments have shown no relevant beneficial results other theories have been postulated to explain the origin of the pathology. The brain is a highly metabolically active energy-consuming tissue in the human body. It has an almost complete dependence on the metabolism of glucose and uses most of its energy for synaptic transmission. Thus, alterations on the utilization or availability of glucose may be cause for the appearance of neurodegenerative pathologies like AD. In this review article, the hypothesis known as Type 3 Diabetes (T3D) will be evaluated by summarizing some of the data that has been reported in recent years. According to published research, the adherence over time to low saturated fatty acids diets in the context of the Mediterranean diet would reduce the inflammatory levels in brain, with a decrease in the pro-inflammatory glial activation and mitochondrial oxidative stress. In this situation, the insulin receptor pathway would be able to fine tune the mitochondrial biogenesis in neuronal cells, regulation the adenosine triphosphate/adenosine diphosphate intracellular balance, and becoming a key factor involved in the preservation of the synaptic connexions and neuronal plasticity. In addition, new targets and strategies for the treatment of AD will be considered in this review for their potential as new pharmacological or non-pharmacological approaches. © Copyright © 2019 Folch, Olloquequi, Ettcheto, Busquets, Sánchez-López, Cano, Espinosa-Jiménez, García, Beas-Zarate, Casadesús, Bulló, Auladell and Camins.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectAlzheimer’s disease
dc.subjectinsulin resistance
dc.subjectMediterranean diet
dc.subjectneuroinflammation and neurodegeneration
dc.subjectobesity
dc.subjecttype 2 diabetes mellitus
dc.subjectadenosine diphosphate
dc.subjectadenosine triphosphate
dc.subjectamyloid beta protein[25-35]
dc.subjectchlorogenic acid
dc.subjectexendin 4
dc.subjectguggul
dc.subjectinsulin
dc.subjectinsulin receptor
dc.subjectinulin
dc.subjectliraglutide
dc.subjectlixisenatide
dc.subjectmemantine
dc.subjectmetformin
dc.subjectperoxisome proliferator activated receptor gamma agonist
dc.subjectpioglitazone
dc.subjectplant medicinal product
dc.subjectsilymarin
dc.subjectsomatomedin C receptor
dc.subjectstress activated protein kinase 1
dc.subjectsulfonylurea derivative
dc.subjectunclassified drug
dc.subjectAlzheimer disease
dc.subjectblood brain barrier
dc.subjectcognition
dc.subjectCurcuma longa
dc.subjectdietary supplement
dc.subjectdisease association
dc.subjectenergy consumption
dc.subjectenzyme activation
dc.subjectfrontal cortex
dc.subjectglia cell
dc.subjectglucose metabolism
dc.subjectglucose utilization
dc.subjecthippocampus
dc.subjecthuman
dc.subjecthypothalamus
dc.subjecthypothesis
dc.subjectinsulin resistance
dc.subjectlipid diet
dc.subjectlong term potentiation
dc.subjectMediterranean diet
dc.subjectmild cognitive impairment
dc.subjectmitochondrial biogenesis
dc.subjectmitochondrion
dc.subjectnerve cell
dc.subjectnerve cell plasticity
dc.subjectneuroprotection
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectobesity
dc.subjectobesogenic diet
dc.subjectoxidative stress
dc.subjectprotein phosphorylation
dc.subjectprotein targeting
dc.subjectReview
dc.subjectrisk factor
dc.subjectsugar intake
dc.subjectsynaptic transmission
dc.subjectWestern diet
dc.titleThe Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer’s Dementia
dc.typeReview


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