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dc.contributor.authorJara C.
dc.contributor.authorAránguiz A.
dc.contributor.authorCerpa W.
dc.contributor.authorTapia-Rojas C.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:20:42Z
dc.date.available2020-09-02T22:20:42Z
dc.date.issued2018
dc.identifier10.1016/j.redox.2018.07.010
dc.identifier.citation18, , 279-294
dc.identifier.issn22132317
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4967
dc.descriptionTau is a key protein for microtubule stability; however, post-translationally modified tau contributes to neurodegenerative diseases by forming tau aggregates in the neurons. Previous reports from our group and others have shown that pathological forms of tau are toxic and impair mitochondrial function, whereas tau deletion is neuroprotective. However, the effects of tau ablation on brain structure and function in young mice have not been fully elucidated. Therefore, the aim of this study was to investigate the implications of tau ablation on the mitochondrial function and cognitive abilities of a litter of young mice (3 months old). Our results showed that tau deletion had positive effects on hippocampal cells by decreasing oxidative damage, favoring a mitochondrial pro-fusion state, and inhibiting mitochondrial permeability transition pore (mPTP) formation by reducing cyclophilin D (Cyp-D) protein. More importantly, tau deletion increased ATP production and improved the recognition memory and attentive capacity of juvenile mice. Therefore, the absence of tau enhanced brain function by improving mitochondrial health, which supplied more energy to the synapses. Thus, our work opens the possibility that preventing negative tau modifications could enhance brain function through the improvement of mitochondrial health. © 2018 The Authors
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectHippocampus
dc.subjectLearning
dc.subjectMemory
dc.subjectMitochondria
dc.subjectTau
dc.subjectadenosine triphosphate
dc.subjectcomplementary DNA
dc.subjectcyclophilin D
dc.subjectmitochondrial permeability transition pore
dc.subjectreduced nicotinamide adenine dinucleotide dehydrogenase (ubiquinone)
dc.subjectRNA
dc.subjecttau protein
dc.subjectubiquinol cytochrome c reductase
dc.subjectcarrier protein
dc.subjectcyclophilin
dc.subjectcyclophilin D
dc.subjectMapt protein, mouse
dc.subjectmitochondrial permeability transition pore
dc.subjecttau protein
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbehavior assessment
dc.subjectbrain cell
dc.subjectcell isolation
dc.subjectcognition
dc.subjectcontrolled study
dc.subjectenzyme activity
dc.subjectgenetic ablation
dc.subjectgenetic procedures
dc.subjecthippocampal slice
dc.subjecthippocampus
dc.subjectmale
dc.subjectmitochondrion
dc.subjectMorris water maze test
dc.subjectmouse
dc.subjectnonhuman
dc.subjectnovel object recognition test
dc.subjectopen field test
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectreal time polymerase chain reaction
dc.subjectrecognition
dc.subjectreverse transcription
dc.subjectRNA extraction
dc.subjectsocial behavior
dc.subjectsocial interaction
dc.subjectsynapse
dc.subjectanimal
dc.subjectgene deletion
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectknockout mouse
dc.subjectlearning
dc.subjectmaze test
dc.subjectmemory
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectphysiology
dc.subjectAnimals
dc.subjectCognition
dc.subjectCyclophilins
dc.subjectGene Deletion
dc.subjectHippocampus
dc.subjectLearning
dc.subjectMale
dc.subjectMaze Learning
dc.subjectMemory
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectMitochondria
dc.subjectMitochondrial Membrane Transport Proteins
dc.subjectOxidative Stress
dc.subjecttau Proteins
dc.titleGenetic ablation of tau improves mitochondrial function and cognitive abilities in the hippocampus
dc.typeArticle


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