NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression. - Wikidata - awgldk - TriplyDB

NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.

NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.

http://www.wikidata.org/entity/Q34764283

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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 Targeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer's disease immunotherapeutics A Metabotropic-Like Flux-Independent NMDA Receptor Regulates Ca2+ Exit from Endoplasmic Reticulum and Mitochondrial Membrane Potential in Cultured Astrocytes Non-Ionotropic NMDA Receptor Signaling Drives Activity-Induced Dendritic Spine Shrinkage.Conformational signaling required for synaptic plasticity by the NMDA receptor complex Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss 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.Local and Use-Dependent Effects of β-Amyloid Oligomers on NMDA Receptor Function Revealed by Optical Quantal Analysis.Ionotropic NMDA receptor signaling is required for the induction of long-term depression in the mouse hippocampal CA1 region.A 'danse macabre': tau and Fyn in STEP with amyloid beta to facilitate induction of synaptic depression and excitotoxicity.Reciprocal disruption of neuronal signaling and Aβ production mediated by extrasynaptic NMDA receptors: a downward spiral.A non-ionotropic activity of NMDA receptors contributes to glycine-induced neuroprotection in cerebral ischemia-reperfusion injury.Biochemical principles underlying the stable maintenance of LTP by the CaMKII/NMDAR complex.Unconventional NMDA Receptor Signaling.Characterizing Gene and Protein Crosstalks in Subjects at Risk of Developing Alzheimer’s Disease: A New Computational Approach Cellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer's Disease

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NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.

http://www.wikidata.org/entity/Q34764283

description

2013 nî lūn-bûn

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2013 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2013 թվականի հունիսին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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name

NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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NMDA-receptor activation but n ...... a induced synaptic depression.

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Albert Tamburri

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Anthony Dudilot

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Catherine Bourgeois

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Jannic Boehm

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Sara Licea

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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

beta-Amyloid(1-42) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer's disease pathology

Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

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

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

Globular amyloid beta-peptide oligomer - a homogenous and stable neuropathological protein in Alzheimer's disease

Regulation of NMDA receptor trafficking by amyloid-beta

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

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

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