Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease. - Wikidata - wikimedia - TriplyDB

Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease.

Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q46463850

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The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease mice The novel cellular mechanism of human 5-HT6 receptor through an interaction with Fyn Abeta-mediated NMDA receptor endocytosis in Alzheimer's disease involves ubiquitination of the tyrosine phosphatase STEP61 Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model.Protein phosphatases and Alzheimer's disease Synapses and Alzheimer's disease Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking Tau Oligomers: The Toxic Player at Synapses in Alzheimer's Disease Genetic reduction of striatal-enriched tyrosine phosphatase (STEP) reverses cognitive and cellular deficits in an Alzheimer's disease mouse model Pathogenesis of synaptic degeneration in Alzheimer's disease and Lewy body disease Amyloid-β induced signaling by cellular prion protein and Fyn kinase in Alzheimer disease The role of tau in neurodegenerative diseases and its potential as a therapeutic target Tau-targeted treatment strategies in Alzheimer's disease Activation of zebrafish Src family kinases by the prion protein is an amyloid-β-sensitive signal that prevents the endocytosis and degradation of E-cadherin/β-catenin complexes in vivo.The dendritic hypothesis for Alzheimer's disease pathophysiology.Striatal-enriched protein tyrosine phosphatase expression and activity in Huntington's disease: a STEP in the resistance to excitotoxicity 5-HT6 receptor antagonists as novel cognitive enhancing agents for Alzheimer's disease Inhibitor of the tyrosine phosphatase STEP reverses cognitive deficits in a mouse model of Alzheimer's disease p21-activated kinase-aberrant activation and translocation in Alzheimer disease pathogenesis Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.Prion protein-mediated toxicity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1 Interfacial water molecules in SH3 interactions: Getting the full picture on polyproline recognition by protein-protein interaction domains.Tyrosine phosphorylation of tau regulates its interactions with Fyn SH2 domains, but not SH3 domains, altering the cellular localization of tau.APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).The developing utility of zebrafish models for cognitive enhancers research Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease.Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice.Uncovering molecular biomarkers that correlate cognitive decline with the changes of hippocampus' gene expression profiles in Alzheimer's disease.Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network.Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein Alzheimer disease models and human neuropathology: similarities and differences Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease.Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease.Synaptic plasticity: one STEP at a time.Premature lethality, hyperactivity, and aberrant phosphorylation in transgenic mice expressing a constitutively active form of Fyn.Progranulin protects against amyloid β deposition and toxicity in Alzheimer's disease mouse models.Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set.Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein

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Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q46463850

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JNEUROSCI.2980-05.2005

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Journal of Neuroscience

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Catherine Massaro

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Eliezer Masliah

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Hilary Gerstein

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Jeannie Chin

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Jorge J Palop

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Jukka Puoliväli

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Kimberly Scearce-Levie

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Lennart Mucke

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Nga Bien-Ly

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9694-9703

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scholarly article

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10.1523/JNEUROSCI.2980-05.2005

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Eliezer Masliah

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2005-10-01T00:00:00Z

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16237174

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Alzheimer's disease

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