A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation. - Wikidata - wikimedia - TriplyDB

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

http://www.wikidata.org/entity/Q37397904

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The human CHRNA7 and CHRFAM7A genes: A review of the genetics, regulation, and function Intraneuronal Aβ accumulation induces hippocampal neuron hyperexcitability through A-type K(+) current inhibition mediated by activation of caspases and GSK-3.The dendritic hypothesis for Alzheimer's disease pathophysiology.Heteromeric α7β2 Nicotinic Acetylcholine Receptors in the Brain Nicotinic ACh receptors as therapeutic targets in CNS disorders Neural Stem Cell Transplant-Induced Effect on Neurogenesis and Cognition in Alzheimer Tg2576 Mice Is Inhibited by Concomitant Treatment with Amyloid-Lowering or Cholinergic α7 Nicotinic Receptor Drugs Depletion of microglia exacerbates postischemic inflammation and brain injury The novel α7β2-nicotinic acetylcholine receptor subtype is expressed in mouse and human basal forebrain: biochemical and pharmacological characterization.Interleukin-17 inhibits adult hippocampal neurogenesis.Evaluation of spinal cord motor function in Alzheimer's disease using electrophysiological techniques indicates association of acetylcholine receptors with the disease.Ly6h regulates trafficking of alpha7 nicotinic acetylcholine receptors and nicotine-induced potentiation of glutamatergic signaling.Neural stem cells sustain natural killer cells that dictate recovery from brain inflammation.The Binding Receptors of Aβ: an Alternative Therapeutic Target for Alzheimer's Disease.Cholinergic System and Post-translational Modifications: An Insight on the Role in Alzheimer's Disease Distinctive Roles for α7*- and α9*-Nicotinic Acetylcholine Receptors in Inflammatory and Autoimmune Responses in the Murine Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models.Epilepsy in patients with Alzheimer's disease: A systematic review.Amyloid β causes excitation/inhibition imbalance through dopamine receptor 1-dependent disruption of fast-spiking GABAergic input in anterior cingulate cortex.Subclinical Doses of ATP-Sensitive Potassium Channel Modulators Prevent Alterations in Memory and Synaptic Plasticity Induced by Amyloid-β.Molecular function of the novel α7β2 nicotinic receptor.Strong Impact of Chronic Cerebral Hypoperfusion on Neurovascular Unit, Cerebrovascular Remodeling, and Neurovascular Trophic Coupling in Alzheimer's Disease Model Mouse.

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A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

http://www.wikidata.org/entity/Q37397904

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on April 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@en

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@nl

type

label

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@en

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@nl

prefLabel

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@en

A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@nl

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JNEUROSCI.3235-12.2013

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Journal of Neuroscience

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A novel nicotinic mechanism underlies β-amyloid-induced neuronal hyperexcitation.

@en

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Jie Wu

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Paul A St John

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Qiang Liu

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Ronald J Lukas

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Xitao Xie

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P2860

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

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Regional distribution of nicotinic receptor subunit mRNAs in human brain: comparison between Alzheimer and normal brain

Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture

Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus.

Loss of alpha7 nicotinic receptors enhances beta-amyloid oligomer accumulation, exacerbating early-stage cognitive decline and septohippocampal pathology in a mouse model of Alzheimer's disease.

Deletion of the alpha 7 nicotinic acetylcholine receptor gene improves cognitive deficits and synaptic pathology in a mouse model of Alzheimer's disease

A simple method for organotypic cultures of nervous tissue

Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function

Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases

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scholarly article

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10.1523/JNEUROSCI.3235-12.2013

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