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dc.contributor.authorEttcheto M.
dc.contributor.authorCano A.
dc.contributor.authorBusquets O.
dc.contributor.authorManzine P.R.
dc.contributor.authorSánchez-López E.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorVerdaguer E.
dc.contributor.authorGarcía M.L.
dc.contributor.authorOlloquequi J.
dc.contributor.authorAuladell C.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:21Z
dc.date.available2020-09-02T22:17:21Z
dc.date.issued2019
dc.identifier10.1016/j.phrs.2019.104255
dc.identifier.citation145, , -
dc.identifier.issn10436618
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4409
dc.descriptionAfter decades of research, the molecular neuropathology of Alzheimer's disease (AD)is still one of the hot topics in biomedical sciences. Some studies suggest that soluble amyloid β (Aβ)oligomers act as causative agents in the development of AD and could be initiators of its complex neurodegenerative cascade. On the other hand, there is also evidence pointing to Aβ oligomers as mere aggravators, with an arguable role in the origin of the disease. In this line of research, the relative contribution of soluble Aβ oligomers to neuronal damage associated with metabolic disorders such as Type 2 Diabetes Mellitus (T2DM)and obesity is being actively investigated. Some authors have proposed the endoplasmic reticulum (ER)stress and the induction of the unfolded protein response (UPR)as important mechanisms leading to an increase in Aβ production and the activation of neuroinflammatory processes. Following this line of thought, these mechanisms could also cause cognitive impairment. The present review summarizes the current understanding on the neuropathological role of Aβ associated with metabolic alterations induced by an obesogenic high fat diet (HFD)intake. It is believed that the combination of these two elements has a synergic effect, leading to the impairement of ER and mitochondrial functions, glial reactivity status alteration and inhibition of insulin receptor (IR)signalling. All these metabolic alterations would favour neuronal malfunction and, eventually, neuronal death by apoptosis, hence causing cognitive impairment and laying the foundations for late-onset AD (LOAD). Moreover, since drugs enhancing the activation of cerebral insulin pathway can constitute a suitable strategy for the prevention of AD, we also discuss the scope of therapeutic approaches such as intranasal administration of insulin in clinical trials with AD patients. © 2019 Elsevier Ltd
dc.language.isoen
dc.publisherAcademic Press
dc.subjectAlzheimer's disease
dc.subjectc-Jun N-terminal kinase inhibitors
dc.subjectInsulin
dc.subjectLicochalcone A
dc.subjectNeuroinflammation
dc.subjectReticulum stress
dc.subjectType 2 diabetes mellitus
dc.subjectamyloid beta protein
dc.subjectanthra[1,9 cd]pyrazol 6(2h) one
dc.subjectantiobesity agent
dc.subjectazeliragon
dc.subjectceramide
dc.subjectchalcone derivative
dc.subjectcholinesterase inhibitor
dc.subjectexendin 4
dc.subjectgastric inhibitory polypeptide
dc.subjectglitazone derivative
dc.subjecthm 15211
dc.subjecthydromethylthionine
dc.subjectinsulin
dc.subjectinsulin detemir
dc.subjectinsulin glulisine
dc.subjectinsulin receptor
dc.subjectlicochalcone A
dc.subjectlicochalcone E
dc.subjectlinolenic acid
dc.subjectliraglutide
dc.subjectlixisenatide
dc.subjectmetformin
dc.subjectpioglitazone
dc.subjectplacebo
dc.subjectquercetin
dc.subjectrosiglitazone
dc.subjectsr 11935
dc.subjectsr 3306
dc.subjectstress activated protein kinase inhibitor
dc.subjectunclassified drug
dc.subjectunindexed drug
dc.subjectamyloid beta protein
dc.subjectceramide
dc.subjectAlzheimer disease
dc.subjectantiinflammatory activity
dc.subjectantineoplastic activity
dc.subjectantioxidant activity
dc.subjectapoptosis
dc.subjectcognitive defect
dc.subjectdisease association
dc.subjectdisorders of mitochondrial functions
dc.subjectdrug efficacy
dc.subjectdrug mechanism
dc.subjectdrug response
dc.subjectdrug safety
dc.subjectendoplasmic reticulum stress
dc.subjectepilepsy
dc.subjecthuman
dc.subjectlipid diet
dc.subjectmetabolic disorder
dc.subjectnerve cell necrosis
dc.subjectnerve degeneration
dc.subjectnervous system inflammation
dc.subjectneuropathology
dc.subjectneuroprotection
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectobesity
dc.subjectpathogenesis
dc.subjectpriority journal
dc.subjectReview
dc.subjectsenile plaque
dc.subjectsignal transduction
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectcognitive defect
dc.subjectcomplication
dc.subjectmetabolism
dc.subjectobesity
dc.subjectAlzheimer Disease
dc.subjectAmyloid beta-Peptides
dc.subjectAnimals
dc.subjectCeramides
dc.subjectCognitive Dysfunction
dc.subjectDiabetes Mellitus, Type 2
dc.subjectEndoplasmic Reticulum Stress
dc.subjectHumans
dc.subjectObesity
dc.titleA metabolic perspective of late onset Alzheimer's disease
dc.typeReview


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