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The implication of the brain insulin receptor in late onset Alzheimer’s disease dementia

dc.contributor.authorFolch J.
dc.contributor.authorEttcheto M.
dc.contributor.authorBusquets O.
dc.contributor.authorSánchez-López E.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorVerdaguer E.
dc.contributor.authorManzine P.R.
dc.contributor.authorPoor S.R.
dc.contributor.authorGarcía M.L.
dc.contributor.authorOlloquequi J.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorAuladell C.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:53Z
dc.date.available2020-09-02T22:17:53Z
dc.date.issued2018
dc.identifier10.3390/ph11010011
dc.identifier.citation11, 1, -
dc.identifier.issn14248247
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4490
dc.descriptionAlzheimer’s disease (AD) is progressive neurodegenerative disorder characterized by brain accumulation of the amyloid β peptide (Aβ), which form senile plaques, neurofibrillary tangles (NFT) and, eventually, neurodegeneration and cognitive impairment. Interestingly, epidemiological studies have described a relationship between type 2 diabetes mellitus (T2DM) and this pathology, being one of the risk factors for the development of AD pathogenesis. Information as it is, it would point out that, impairment in insulin signalling and glucose metabolism, in central as well as peripheral systems, would be one of the reasons for the cognitive decline. Brain insulin resistance, also known as Type 3 diabetes, leads to the increase of Aβ production and TAU phosphorylation, mitochondrial dysfunction, oxidative stress, protein misfolding, and cognitive impairment, which are all hallmarks of AD. Moreover, given the complexity of interlocking mechanisms found in late onset AD (LOAD) pathogenesis, more data is being obtained. Recent evidence showed that Aβ42 generated in the brain would impact negatively on the hypothalamus, accelerating the “peripheral” symptomatology of AD. In this situation, Aβ42 production would induce hypothalamic dysfunction that would favour peripheral hyperglycaemia due to down regulation of the liver insulin receptor. The objective of this review is to discuss the existing evidence supporting the concept that brain insulin resistance and altered glucose metabolism play an important role in pathogenesis of LOAD. Furthermore, we discuss AD treatment approaches targeting insulin signalling using anti-diabetic drugs and mTOR inhibitors. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectAlzheimer’s
dc.subjectAmyloid
dc.subjectCognition
dc.subjectInsulin receptor
dc.subjectInsulin resistance
dc.subjectTAU
dc.subjectType 2 diabetes
dc.subjectamyloid beta protein[1-42]
dc.subjectantidiabetic agent
dc.subjectbeta secretase 1
dc.subjectglucose transporter 4
dc.subjectinsulin
dc.subjectinsulin receptor
dc.subjectinsulinase
dc.subjectmammalian target of rapamycin inhibitor
dc.subjectoligomer
dc.subjectprotein kinase B
dc.subjecttau protein
dc.subjecttranscription factor FOXO
dc.subjectAlzheimer disease
dc.subjectArticle
dc.subjectcognition
dc.subjectdementia
dc.subjectdisease association
dc.subjectdown regulation
dc.subjectglucose metabolism
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjecthypothalamus disease
dc.subjectinsulin resistance
dc.subjectinsulin signaling
dc.subjectnerve degeneration
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectoutcome assessment
dc.subjectpathogenesis
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectprotein phosphorylation
dc.subjecttotal quality management
dc.titleThe implication of the brain insulin receptor in late onset Alzheimer’s disease dementia
dc.typeArticle


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