Spatial memory impairment is associated with intraneural amyloid-? immunoreactivity and dysfunctional arc expression in the hippocampal-CA3 region of a transgenic mouse model of Alzheimer’s disease

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dc.audience researchers es_MX
dc.contributor.author Jean-Pascal Morin, 0000-0001-8221-4982
dc.contributor.author Gustavo Pacheco-Lopez, 0000-0002-3458-197X
dc.contributor.author Federico Bermudez_Rattoni, 0000-0003-2056-6119
dc.contributor.other Cerón Solano, Giovanni
dc.contributor.other Velázquez Campos, Giovanna
dc.contributor.other Díaz Cintra, Sofía
dc.coverage MX es_MX
dc.date.accessioned 2018-06-27T02:32:40Z
dc.date.available 2018-06-27T02:32:40Z
dc.date.issued 2016
dc.description Dysfunction of synaptic communication in cortical and hippocampal networks has been suggested as one of the neuropathological hallmarks of the early stages of Alzheimer’s disease (AD). Also, several lines of evidence have linked disrupted levels of activity-regulated cytoskeletal associated protein (Arc), an immediate early gene product that plays a central role in synaptic plasticity, with AD “synaptopathy”. The mapping of Arc expression patterns in brain networks has been extensively used as a marker of memory-relevant neuronal activity history. Here we evaluated basal and behavior-induced Arc expression in hippocampal networks of the 3xTg-AD mouse model of AD. The basal percentage of Arc-expressing cells in 10-month-old 3xTg-AD mice was higher than wild type in CA3 (4.88% versus 1.77% , respectively) but similar in CA1 (1.75% versus 2.75% ). Noteworthy, this difference was not observed at 3 months of age. Furthermore, although a Morris water maze test probe induced a steep (∼4-fold) increment in the percentage of Arc+ cells in the CA3 region of the 10-month-old wild-type group, no such increment was observed in age-matched 3xTg-AD, whereas the amount of Arc+ cells in CA1 increased in both groups. Further, we detected that CA3 neurons with amyloid-β were much more likely to express Arc protein under basal conditions. We propose that in 3xTg-AD mice, intraneuronal amyloid-β expression in CA3 could increase unspecific neuronal activation and subsequent Arc protein expression, which might impair further memory-stabilizing processes. es_MX
dc.format application/pdf es_MX
dc.identificador.materia 3 es_MX
dc.identifier.uri http://hdl.handle.net/20.500.12222/172
dc.language eng es_MX
dc.publisher Universidad Autónoma Metropolitana. Unidad Lerma es_MX
dc.rights Attribution-NonCommercial-NoDerivatives 4.0 Internacional *
dc.rights.license info:eu-repo/semantics/openAccess *
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/4.0/ es_MX
dc.subject MEDICINA Y CIENCIAS DE LA SALUD es_MX
dc.subject.keywords Activity Regulated Cytoskeletal es_MX
dc.subject.keywords Associated Protein es_MX
dc.subject.keywords Alzheimer’s Disease es_MX
dc.subject.keywords Hippocampus es_MX
dc.subject.keywords Memory es_MX
dc.subject.keywords Neuroplasticity es_MX
dc.title Spatial memory impairment is associated with intraneural amyloid-? immunoreactivity and dysfunctional arc expression in the hippocampal-CA3 region of a transgenic mouse model of Alzheimer’s disease es_MX
dc.type preprint es_MX
dc.type.version info:eu-repo/semantics/publishedVersion es_MX
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