Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss - Wikidata - wikimedia - TriplyDB

Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss

Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss

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Therapies for Prevention and Treatment of Alzheimer's Disease The Emergence of NMDA Receptor Metabotropic Function: Insights from Imaging Non-ionotropic signaling by the NMDA receptor: controversy and opportunity Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking Tau Biology and Tau-Directed Therapies for Alzheimer's Disease Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture.Non-Ionotropic NMDA Receptor Signaling Drives Activity-Induced Dendritic Spine Shrinkage.Glycine triggers a non-ionotropic activity of GluN2A-containing NMDA receptors to confer neuroprotection.Glycine Potentiates AMPA Receptor Function through Metabotropic Activation of GluN2A-Containing NMDA Receptors.Dehydroevodiamine·HCl enhances cognitive function in memory-impaired rat models.Separate Ionotropic and Metabotropic Glutamate Receptor Functions in Depotentiation vs. LTP: A Distinct Role for Group1 mGluR Subtypes and NMDARs.Biometal Dyshomeostasis and Toxic Metal Accumulations in the Development of Alzheimer's Disease.Unconventional NMDA Receptor Signaling.Therapeutics of Neurotransmitters in Alzheimer's Disease.Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

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Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss

http://www.wikidata.org/entity/Q36347364

description

2015 nî lūn-bûn

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2015年の論文

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年學術文章

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2015年學術文章

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name

Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

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Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

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type

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Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

@ast

Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

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prefLabel

Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

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Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

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Calcium flux-independent NMDA ...... oligomer-induced synaptic loss

@en

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J Bali

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J H Birnbaum

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R M Nitsch

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P2860

A Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease

Paradigm shift in neuroprotection by NMDA receptor blockade: Memantine and beyond

Memantine preferentially blocks extrasynaptic over synaptic NMDA receptor currents in hippocampal autapses

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

p38 activation is required upstream of potassium current enhancement and caspase cleavage in thiol oxidant-induced neuronal apoptosis

Rap1-induced p38 mitogen-activated protein kinase activation facilitates AMPA receptor trafficking via the GDI.Rab5 complex. Potential role in (S)-3,5-dihydroxyphenylglycene-induced long term depression

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

Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine.

Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment

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e1791

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scholarly article

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10.1038/CDDIS.2015.160

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6

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Lawrence Rajendran

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2015-06-18T00:00:00Z

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278790297

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1038231992

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26086964

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4669839

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