Cargando…

Progressive Changes in Sleep and Its Relations to Amyloid-β Distribution and Learning in Single App Knock-In Mice

Alzheimer’s disease (AD) patients often suffer from sleep disturbances. Alterations in sleep, especially rapid eye movement sleep (REMS), can precede the onset of dementia. To accurately characterize the sleep impairments accompanying AD and their underlying mechanisms using animal models, it is cru...

Descripción completa

Detalles Bibliográficos
Autores principales:	Maezono, Sakura Eri B., Kanuka, Mika, Tatsuzawa, Chika, Morita, Miho, Kawano, Taizo, Kashiwagi, Mitsuaki, Nondhalee, Pimpimon, Sakaguchi, Masanori, Saito, Takashi, Saido, Takaomi C., Hayashi, Yu
Formato:	Online Artículo Texto
Lenguaje:	English
Publicado:	Society for Neuroscience 2020
Materias:	Research Article: New Research
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7196722/ https://www.ncbi.nlm.nih.gov/pubmed/32321771 http://dx.doi.org/10.1523/ENEURO.0093-20.2020

Ejemplares similares

Impaired wakefulness and rapid eye movement sleep in dopamine-deficient mice
por: Kashiwagi, Mitsuaki, et al.
Publicado: (2021)

Analysis of Taste Sensitivities in App Knock-In Mouse Model of Alzheimer’s Disease
por: Narukawa, Masataka, et al.
Publicado: (2020)

Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis
por: Sakakibara, Yasufumi, et al.
Publicado: (2018)

The senile plaque: Morphological differences in APP knock‐in mice brains by fixatives
por: Yoshimura, Rikuya, et al.
Publicado: (2023)

Presubiculum principal cells are preserved from degeneration in knock-in APP/TAU mouse models of Alzheimer’s disease
por: Islam, Anam, et al.
Publicado: (2023)

Generation of App knock-in mice reveals deletion mutations protective against Alzheimer’s disease-like pathology
por: Nagata, Kenichi, et al.
Publicado: (2018)

Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease
por: Sakakibara, Yasufumi, et al.
Publicado: (2019)

The two faces of synaptic failure in App(NL-G-F) knock-in mice
por: Latif-Hernandez, Amira, et al.
Publicado: (2020)

Neuronal Cell Cycle Re-Entry Enhances Neuropathological Features in App(NLF) Knock-In Mice
por: Barrett, Tomás, et al.
Publicado: (2021)

Increased Insoluble Amyloid-β Induces Negligible Cognitive Deficits in Old App(NL/NL) Knock-In Mice
por: Salas, Isabel H., et al.
Publicado: (2018)

Contribution of GABAergic interneurons to amyloid-β plaque pathology in an APP knock-in mouse model
por: Rice, Heather C., et al.
Publicado: (2020)

Widespread Reduced Density of Noradrenergic Locus Coeruleus Axons in the App Knock-In Mouse Model of Amyloid-β Amyloidosis
por: Sakakibara, Yasufumi, et al.
Publicado: (2021)

Amelioration of Alzheimer’s Disease by Gut-Pancreas-Liver-Brain Interaction in an App Knock-In Mouse Model
por: Minamisawa, Mayumi, et al.
Publicado: (2021)

An isogenic panel of App knock-in mouse models: Profiling β-secretase inhibition and endosomal abnormalities
por: Watamura, Naoto, et al.
Publicado: (2022)

Proteomic alterations in the brain and blood–brain barrier during brain Aβ accumulation in an APP knock-in mouse model of Alzheimer’s disease
por: Ito, Shingo, et al.
Publicado: (2023)

Hippocampal functional connectivity across age in an App knock-in mouse model of Alzheimer's disease
por: Morrissey, Zachery D., et al.
Publicado: (2023)

A high‐fat diet exacerbates the Alzheimer's disease pathology in the hippocampus of the App (NL−F/NL−F) knock‐in mouse model
por: Mazzei, Guianfranco, et al.
Publicado: (2021)

Cerebellar control of fear learning via the cerebellar nuclei–Multiple pathways, multiple mechanisms?
por: Urrutia Desmaison, Julie D., et al.
Publicado: (2023)

Insoluble Aβ overexpression in an App knock-in mouse model alters microstructure and gamma oscillations in the prefrontal cortex, affecting anxiety-related behaviours
por: Pervolaraki, Eleftheria, et al.
Publicado: (2019)

Spatial reversal learning defect coincides with hypersynchronous telencephalic BOLD functional connectivity in APP(NL-F/NL-F) knock-in mice
por: Shah, Disha, et al.
Publicado: (2018)

Age-Dependent Behavioral and Metabolic Assessment of App(NL−G−F/NL−G−F) Knock-in (KI) Mice
por: Wang, Shanshan, et al.
Publicado: (2022)

Proteomics Time-Course Study of App Knock-In Mice Reveals Novel Presymptomatic Aβ(42)-Induced Pathways to Alzheimer’s Disease Pathology
por: Schedin-Weiss, Sophia, et al.
Publicado: (2020)

An impaired intrinsic microglial clock system induces neuroinflammatory alterations in the early stage of amyloid precursor protein knock-in mouse brain
por: Ni, Junjun, et al.
Publicado: (2019)

Touchscreen-based location discrimination and paired associate learning tasks detect cognitive impairment at an early stage in an App knock-in mouse model of Alzheimer’s disease
por: Saifullah, Md. Ali Bin, et al.
Publicado: (2020)

Early memory deficits and extensive brain network disorganization in the App(NL-F)/MAPT double knock-in mouse model of familial Alzheimer’s disease
por: Borcuk, Christopher, et al.
Publicado: (2022)

Behavioral and neuropathological characterization over the adult lifespan of the human tau knock-in mouse
por: Benskey, Matthew J., et al.
Publicado: (2023)

Increase in Tau Pathology in P290S Mapt Knock-In Mice Crossed with App(NL-G-F) Mice
por: Huang, Melissa, et al.
Publicado: (2022)

Cerebral Aβ deposition precedes reduced cerebrospinal fluid and serum Aβ42/Aβ40 ratios in the App(NL−F/NL−F) knock-in mouse model of Alzheimer’s disease
por: Andersson, Emelie, et al.
Publicado: (2023)

Endothelial expression of human amyloid precursor protein leads to amyloid β in the blood and induces cerebral amyloid angiopathy in knock-in mice
por: Tachida, Yuriko, et al.
Publicado: (2022)

Novel Quantitative Analyses of Spontaneous Synaptic Events in Cortical Pyramidal Cells Reveal Subtle Parvalbumin-Expressing Interneuron Dysfunction in a Knock-In Mouse Model of Alzheimer’s Disease
por: Chen, Lingxuan, et al.
Publicado: (2018)

Impaired In Vivo Gamma Oscillations in the Medial Entorhinal Cortex of Knock-in Alzheimer Model
por: Nakazono, Tomoaki, et al.
Publicado: (2017)

T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice
por: Wang, Shuo, et al.
Publicado: (2018)

Highly improved cloning efficiency for plasmid-based CRISPR knock-in in C. elegans
por: DeMott, Ella, et al.
Publicado: (2021)

Correction: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice
por: Wang, Shuo, et al.
Publicado: (2019)

Phenotypic Differences between the Alzheimer’s Disease-Related hAPP-J20 Model and Heterozygous Zbtb20 Knock-Out Mice
por: Gulbranson, Daniel R., et al.
Publicado: (2021)

Impaired sharp-wave ripple coordination between the medial entorhinal cortex and hippocampal CA1 of knock-in model of Alzheimer’s disease
por: Funane, Tsukasa, et al.
Publicado: (2022)

Metabolism of amyloid β peptide and pathogenesis of Alzheimer’s disease
por: SAIDO, Takaomi C.
Publicado: (2013)

An nhr-23::mScarlet::3xMyc knock-in allele for studying spermatogenesis and molting
por: Myles, Krista M., et al.
Publicado: (2023)

Using CRISPR knock-in of fluorescent tags to examine isoform-specific expression of EGL-19 in C. elegans
por: McDonald, Kara, et al.
Publicado: (2023)

Impairment in novelty-promoted memory via behavioral tagging and capture before apparent memory loss in a knock-in model of Alzheimer’s disease
por: Broadbelt, Tabitha, et al.
Publicado: (2022)

Cannot write session to /tmp/vufind_sessions/sess_5t0fonbc12uars5sducbk65hp5