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dc.contributor.authorVerdaguer E.
dc.contributor.authorBrox S.
dc.contributor.authorPetrov D.
dc.contributor.authorOlloquequi J.
dc.contributor.authorRomero R.
dc.contributor.authorde Lemos M.L.
dc.contributor.authorCamins A.
dc.contributor.authorAuladell C.
dc.date.accessioned2020-09-02T22:30:01Z
dc.date.available2020-09-02T22:30:01Z
dc.date.issued2015
dc.identifier10.1016/j.exger.2015.06.013
dc.identifier.citation69, , 176-188
dc.identifier.issn05315565
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6549
dc.descriptionThe pathogenesis of Alzheimer disease (AD) is characterized by accumulation of β-amyloid protein in the brain (in both soluble and insoluble forms) and by the presence of intracellular neurofibrillary tangles (NFTs), leading to neurotoxicity. The exact mechanisms whereby Aβ triggers brain alterations are unclear. However, accumulating evidence suggests that a deregulation of Ca2+ signaling may play a major role in disease progression. Calcium-buffering proteins, including calbindin-D28K (CB), calretinin (CR) and parvalbumin (PV), may offer neuroprotection by maintaining calcium homeostasis. Although marked reductions in these proteins have been observed in the brains of mice and humans with AD, their contribution to AD pathology remains unclear. The aim of the present study was to analyze distribution patterns of CB+, CR+ and PV+ interneurons in different areas of the hippocampus, a brain region that is severely affected in AD. A transgenic knock-in APPswe/PS1dE9 mouse model of familial AD was used. The data were obtained from the brains of 3- and 12-month-old animals. These ages roughly correspond to an early mature adult (prior to clinical manifestations) and a late middle-age (clinical symptoms readily detectable) phase in human AD patients. Immunostaining revealed increases in CB and PV immunoreactivity (IR) in the hippocampus of 3-month-old transgenic mice, compared to wild-type animals. Possibly, these proteins are upregulated in an attempt to control cellular homeostasis and synaptic plasticity. However, the pattern of CB-IR was reversed in 12-month-old animals, potentially indicating a loss of cellular capacity to respond to pathophysiological processes. In addition, at this age, a noticeable increase in PV-IR was observed, suggesting the presence of hippocampal network hyperactivity in older AD-like mice. Our results indicate that CaBP+ neuronal subpopulations play a role in adult neurogenesis and in AD pathology, particularly at early disease stages, suggesting that these neurons may serve as potential predictors of future AD in non-demented individuals. © 2015 Elsevier Inc..
dc.language.isoen
dc.publisherElsevier Inc.
dc.subjectAlzheimer disease
dc.subjectAPPswe/PS1dE9 mouse
dc.subjectCalbindin
dc.subjectCalretinin
dc.subjectHippocampus
dc.subjectParvalbumin
dc.subjectcalbindin
dc.subjectcalretinin
dc.subjectdoublecortin
dc.subjectneuron specific nuclear protein
dc.subjectparvalbumin
dc.subjectcalbindin
dc.subjectcalretinin
dc.subjectparvalbumin
dc.subjectAlzheimer disease
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectAPPswe mouse
dc.subjectArticle
dc.subjectbrain tissue
dc.subjectcell metabolism
dc.subjectcellular distribution
dc.subjectclinical feature
dc.subjectcontrolled study
dc.subjectdentate gyrus
dc.subjecthippocampal CA1 region
dc.subjecthippocampal CA3 region
dc.subjecthippocampus
dc.subjectimmunohistochemistry
dc.subjectimmunoreactivity
dc.subjectinterneuron
dc.subjectmale
dc.subjectmouse
dc.subjectmouse strain
dc.subjectnerve cell network
dc.subjectnerve cell plasticity
dc.subjectnervous system development
dc.subjectneuropathology
dc.subjectnonhuman
dc.subjectpathophysiology
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectPS1dE9 mouse
dc.subjecttransgenic mouse
dc.subjectupregulation
dc.subjectwild type mouse
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectdisease course
dc.subjectdisease model
dc.subjectmetabolism
dc.subjectnerve conduction
dc.subjectnervous system development
dc.subjectneurofibrillary tangle
dc.subjectpathology
dc.subjectphysiology
dc.subjectAlzheimer Disease
dc.subjectAnimals
dc.subjectCalbindin 2
dc.subjectCalbindins
dc.subjectDisease Models, Animal
dc.subjectDisease Progression
dc.subjectHippocampus
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectNeural Conduction
dc.subjectNeurofibrillary Tangles
dc.subjectNeurogenesis
dc.subjectNeuronal Plasticity
dc.subjectParvalbumins
dc.titleVulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis
dc.typeArticle


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