Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease - Wikidata - awgldk - TriplyDB

Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease

Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease

http://www.wikidata.org/entity/Q33707872

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Toward more predictive genetic mouse models of Alzheimer's disease Transnasal delivery of human A-beta peptides elicits impaired learning and memory performance in wild type mice.Impaired Recall of Positional Memory following Chemogenetic Disruption of Place Field Stability.Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities Alzheimer's therapeutics targeting amyloid beta 1-42 oligomers I: Abeta 42 oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits Corticotropin-releasing factor receptor-1 antagonism mitigates beta amyloid pathology and cognitive and synaptic deficits in a mouse model of Alzheimer's disease.Scanning ultrasound removes amyloid-β and restores memory in an Alzheimer's disease mouse model.Amyloid-β pathology and APOE genotype modulate retinoid X receptor agonist activity in vivo.Design of donecopride, a dual serotonin subtype 4 receptor agonist/acetylcholinesterase inhibitor with potential interest for Alzheimer's disease treatment.Longitudinal testing of hippocampal plasticity reveals the onset and maintenance of endogenous human Aß-induced synaptic dysfunction in individual freely behaving pre-plaque transgenic rats: rapid reversal by anti-Aß agents.APOE4 enhances age-dependent decline in cognitive function by down-regulating an NMDA receptor pathway in EFAD-Tg mice.Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease Quaternary Structure Defines a Large Class of Amyloid-β Oligomers Neutralized by Sequestration.Humanized Tau Mice with Regionalized Amyloid Exhibit Behavioral Deficits but No Pathological Interaction.Phosphorylation of Tyrosine 1070 at the GluN2B Subunit Is Regulated by Synaptic Activity and Critical for Surface Expression of N-Methyl-D-aspartate (NMDA) Receptors What amyloid ligands can tell us about molecular polymorphism and disease.Deletion of the type-1 interferon receptor in APPSWE/PS1ΔE9 mice preserves cognitive function and alters glial phenotype Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer's disease.The neurotoxicity of amyloid β-protein oligomers is reversible in a primary neuron model.Toxic oligomer species of amyloid-β in Alzheimer's disease, a timing issue.Antibody-based PET imaging of amyloid beta in mouse models of Alzheimer's disease Cellular Regulation of Amyloid Formation in Aging and Disease.Bivalent Brain Shuttle Increases Antibody Uptake by Monovalent Binding to the Transferrin Receptor.Reversal of Synapse Degeneration by Restoring Wnt Signaling in the Adult Hippocampus.NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer's disease.Discrete pools of oligomeric amyloid-β track with spatial learning deficits in a mouse model of Alzheimer amyloidosis.The amyloid-β oligomer Aβ*56 induces specific alterations in neuronal signaling that lead to tau phosphorylation and aggregation.Practical considerations for choosing a mouse model of Alzheimer's disease.Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP.Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease.Combination anti-Aβ treatment maximizes cognitive recovery and rebalances mTOR signaling in APP mice.7B2 chaperone knockout in APP model mice results in reduced plaque burden.Origin of metastable oligomers and their effects on amyloid fibril self-assembly

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Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease

http://www.wikidata.org/entity/Q33707872

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2014 nî lūn-bûn

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2014 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2014年の論文

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JNEUROSCI.0572-14.2014

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Journal of Neuroscience

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Genetic modulation of soluble ...... e model of Alzheimer's disease

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Angie C A Chiang

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Dorothy R Schuler

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Joanna L Jankowsky

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John R Cirrito

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Mathew A Sherman

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Megan E Larson

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Stephanie W Fowler

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P2860

Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease

Passive immunotherapy against Abeta in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage

Spines, plasticity, and cognition in Alzheimer's model mice

PAK in Alzheimer disease, Huntington disease and X-linked mental retardation

p21-activated kinase-aberrant activation and translocation in Alzheimer disease pathogenesis

Reversible memory loss in a mouse transgenic model of Alzheimer's disease

Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway

A specific amyloid-beta protein assembly in the brain impairs memory

Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis

Control of memory formation through regulated expression of a CaMKII transgene

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10.1523/JNEUROSCI.0572-14.2014

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23

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Sylvain E Lesné

Ricky R Savjani

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Alzheimer's disease

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