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c-Jun N-terminal Kinase 1 ablation protects against metabolic-induced hippocampal cognitive impairments

dc.contributor.authorBusquets O.
dc.contributor.authorEttcheto M.
dc.contributor.authorEritja À.
dc.contributor.authorEspinosa-Jiménez T.
dc.contributor.authorVerdaguer E.
dc.contributor.authorOlloquequi J.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorCasadesús G.
dc.contributor.authorAuladell C.
dc.contributor.authorBulló M.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:13:36Z
dc.date.available2020-09-02T22:13:36Z
dc.date.issued2019
dc.identifier10.1007/s00109-019-01856-z
dc.identifier.citation97, 12, 1723-1733
dc.identifier.issn09462716
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3809
dc.descriptionAbstract: The development of metabolic alterations like insulin resistance has been associated with dysfunctions in mitochondrial oxidative capacity, induction of neuroinflammatory responses, and the appearance of cognitive impairments in the brain. The c-Jun N-terminal Kinase 1 (JNK1) is a potential key modulator of these mechanisms. The current study identifies a protective effect of whole-body JNK1 knockout in the presence of a high-fat diet (HFD). Specifically, the data suggest that mice missing JNK1 show increased insulin sensitivity and mitochondrial activity, as well as reduced body weight, and astrocyte and microglial reactivity. Finally, these animals are also protected against HFD-induced cognitive impairments as assessed through novel object recognition test, the observation of dendritic spines, and the levels of BDNF or other proteins like spinophilin and ARC. Thus, modulation of JNK1 activity seems like a promising approach for the design of therapies aimed at treating metabolic-induced cognitive impairments. Key messages: JNK1 is a link between obesity/type 2 diabetes and cognitive lossInhibition of JNK1 is neuroprotectiveJNK1 constitutes a therapeutic strategy for cognitive loss. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
dc.language.isoen
dc.publisherSpringer
dc.subjectc-Jun N-terminal Kinase 1
dc.subjectCognitive impairments
dc.subjectHigh-fat diet
dc.subjectbrain derived neurotrophic factor
dc.subjectcitrate synthase
dc.subjectspinophilin
dc.subjectstress activated protein kinase 1
dc.subjectactin binding protein
dc.subjectbrain derived neurotrophic factor
dc.subjectnerve protein
dc.subjectneurabin
dc.subjectstress activated protein kinase 1
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectantioxidant activity
dc.subjectArticle
dc.subjectastrocyte
dc.subjectbody weight
dc.subjectcognitive defect
dc.subjectcomparative study
dc.subjectcontrolled study
dc.subjectdendritic spine
dc.subjectdisease association
dc.subjectenzyme activity
dc.subjectfat content
dc.subjectglucose tolerance test
dc.subjectGolgi stain
dc.subjectimmunofluorescence
dc.subjectinsulin resistance
dc.subjectinsulin sensitivity
dc.subjectinsulin tolerance test
dc.subjectlipid diet
dc.subjectlong term care
dc.subjectlong term exposure
dc.subjectmale
dc.subjectmetabolic disorder
dc.subjectmotor activity
dc.subjectmouse
dc.subjectneuromodulation
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectnovel object recognition test
dc.subjectobservation
dc.subjectoxidative phosphorylation
dc.subjectreal time polymerase chain reaction
dc.subjectWestern blotting
dc.subjectadverse event
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectcognition assessment
dc.subjectcognitive defect
dc.subjectcomplication
dc.subjectenzymology
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectmicroglia
dc.subjectmitochondrion
dc.subjectphysiology
dc.subjecttransgenic mouse
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectBody Weight
dc.subjectBrain-Derived Neurotrophic Factor
dc.subjectCognitive Dysfunction
dc.subjectDendritic Spines
dc.subjectDiabetes Mellitus, Type 2
dc.subjectDiet, High-Fat
dc.subjectHippocampus
dc.subjectInsulin Resistance
dc.subjectMale
dc.subjectMemory and Learning Tests
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Transgenic
dc.subjectMicrofilament Proteins
dc.subjectMicroglia
dc.subjectMitochondria
dc.subjectMitogen-Activated Protein Kinase 8
dc.subjectNerve Tissue Proteins
dc.titlec-Jun N-terminal Kinase 1 ablation protects against metabolic-induced hippocampal cognitive impairments
dc.typeArticle


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