mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo
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Amyloid-β-Induced Dysregulation of AMPA Receptor TraffickingThe biological function of the cellular prion protein: an updateAmyloid β Protein and Alzheimer's Disease: When Computer Simulations Complement Experimental Studies.Therapeutic molecules and endogenous ligands regulate the interaction between brain cellular prion protein (PrPC) and metabotropic glutamate receptor 5 (mGluR5).Cellular prion protein and NMDA receptor modulation: protecting against excitotoxicity.A human monoclonal IgG that binds aβ assemblies and diverse amyloids exhibits anti-amyloid activities in vitro and in vivo.Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's diseaseTherapeutic potential of mGluR5 targeting in Alzheimer's diseasePrion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models.Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic lossMetabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's diseaseRepression of the eIF2α kinase PERK alleviates mGluR-LTD impairments in a mouse model of Alzheimer's diseaseAPP Causes Hyperexcitability in Fragile X Mice.Large Soluble Oligomers of Amyloid β-Protein from Alzheimer Brain Are Far Less Neuroactive Than the Smaller Oligomers to Which They Dissociate.The Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling ModulesGlutamate receptors function as scaffolds for the regulation of β-amyloid and cellular prion protein signaling complexes.Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer's Mouse Phenotypes.High-Resolution Structures of the Amyloid-β 1-42 Dimers from the Comparison of Four Atomistic Force Fields.Group I Metabotropic Glutamate Receptor Interacting Proteins: Fine-Tuning Receptor Functions in Health and Disease.Amyloid-β Oligomers Interact with Neurexin and Diminish Neurexin-mediated Excitatory Presynaptic Organization.Cellular prion protein as a receptor for amyloid-β oligomers in Alzheimer's disease.Binding Sites for Amyloid-β Oligomers and Synaptic Toxicity.Interactions of pathological proteins in neurodegenerative diseases.Role of amyloid β protein receptors in mediating synaptic plasticity.Acute intracerebral treatment with amyloid-beta (1-42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in freely behaving rats.Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 Complex.Somatostatin binds to the human amyloid β peptide and favors the formation of distinct oligomers.Age-Dependent Long-Term Potentiation Deficits in the Prefrontal Cortex of the Fmr1 Knockout Mouse Model of Fragile X Syndrome.Lipid rafts: linking prion protein to zinc transport and amyloid-β toxicity in Alzheimer's diseaseIdentification of a Compound That Disrupts Binding of Amyloid-β to the Prion Protein Using a Novel Fluorescence-based Assay.Inhibition of group-I metabotropic glutamate receptors protects against prion toxicity.Soluble Aβ aggregates can inhibit prion propagation.Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease.Opposite in vivo effects of agents that stimulate or inhibit the glutamate/cysteine exchanger system xc- on the inhibition of hippocampal LTP by Aß.Peripheral Interventions Enhancing Brain Glutamate Homeostasis Relieve Amyloid β- and TNFα- Mediated Synaptic Plasticity Disruption in the Rat Hippocampus.Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.Synaptotoxic Signaling by Amyloid Beta Oligomers in Alzheimer's Disease Through Prion Protein and mGluR5.Physiological activation of mGlu5 receptors supports the ion channel function of NMDA receptors in hippocampal LTD induction in vivo.Extracellular Forms of Aβ and Tau from iPSC Models of Alzheimer's Disease Disrupt Synaptic Plasticity.
P2860
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P2860
mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo
description
2014 nî lūn-bûn
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2014 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի մարտին հրատարակված գիտական հոդված
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2014年の論文
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2014年論文
@yue
2014年論文
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2014年論文
@zh-hk
2014年論文
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2014年論文
@zh-tw
2014年论文
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name
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@ast
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@en
type
label
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@ast
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@en
prefLabel
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@ast
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@en
P2093
P2860
P50
P356
P1476
mGlu5 receptors and cellular p ...... c long-term depression in vivo
@en
P2093
Andrew J Nicoll
Dainan Zhang
Dominic M Walsh
John Collinge
Silvia A Purro
P2860
P2888
P356
10.1038/NCOMMS4374
P407
P577
2014-03-04T00:00:00Z