Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers. - Wikidata - wikimedia - TriplyDB

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

http://www.wikidata.org/entity/Q35126030

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Widespread distribution of reticulon-3 in various neurodegenerative diseases Synthetic amyloid-beta oligomers impair long-term memory independently of cellular prion protein Tau Oligomers: The Toxic Player at Synapses in Alzheimer's Disease Targeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer's disease immunotherapeutics Alzheimer's disease and insulin resistance: translating basic science into clinical applications The role of tau in neurodegenerative diseases and its potential as a therapeutic target RPS23RG1 reduces Aβ oligomer-induced synaptic and cognitive deficits.Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students Spreading of pathology in neurodegenerative diseases: a focus on human studies Lipid microdomain modification sustains neuronal viability in models of Alzheimer's disease PAK in Alzheimer disease, Huntington disease and X-linked mental retardation Amyloid-β triggers the release of neuronal hexokinase 1 from mitochondria Protection of synapses against Alzheimer's-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers Synaptic protein α1-takusan mitigates amyloid-β-induced synaptic loss via interaction with tau and postsynaptic density-95 at postsynaptic sites Protection against the synaptic targeting and toxicity of Alzheimer's-associated Aβ oligomers by insulin mimetic chiro-inositols.Biophysical insights into how surfaces, including lipid membranes, modulate protein aggregation related to neurodegeneration.Cytoskeletal pathologies of Alzheimer disease β-Amyloid impairs axonal BDNF retrograde trafficking.Amyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neurons Dendritic and axonal mechanisms of Ca2+ elevation impair BDNF transport in Aβ oligomer-treated hippocampal neurons Human neural stem cells alleviate Alzheimer-like pathology in a mouse model.Early and progressive deficit of neuronal activity patterns in a model of local amyloid pathology in mouse prefrontal cortex Alzheimer's-associated Abeta oligomers show altered structure, immunoreactivity and synaptotoxicity with low doses of oleocanthal.Structure-function relationships of pre-fibrillar protein assemblies in Alzheimer's disease and related disorders Point mutations in Aβ result in the formation of distinct polymorphic aggregates in the presence of lipid bilayers.Tg2576 cortical neurons that express human Ab are susceptible to extracellular Aβ-induced, K+ efflux dependent neurodegeneration Discovery of 5-(4-hydroxyphenyl)-3-oxo-pentanoic acid [2-(5-methoxy-1H-indol-3-yl)-ethyl]-amide as a neuroprotectant for Alzheimer's disease by hybridization of curcumin and melatonin Staging of Alzheimer's pathology in triple transgenic mice: a light and electron microscopic analysis.GSK3β is involved in the relief of mitochondria pausing in a Tau-dependent manner Disordered amyloidogenic peptides may insert into the membrane and assemble into common cyclic structural motifs.The neuroprotective effect of Klotho is mediated via regulation of members of the redox system.Design of β-amyloid aggregation inhibitors from a predicted structural motif.Alzheimer's disease: which type of amyloid-preventing drug agents to employ?Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease.Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.Prophylaxis and treatment of Alzheimer's disease by delivery of an adeno-associated virus encoding a monoclonal antibody targeting the amyloid Beta protein.Suppressed retinal degeneration in aged wild type and APPswe/PS1ΔE9 mice by bone marrow transplantation Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo.Sinomenine inhibits microglial activation by Aβ and confers neuroprotection.

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P2860

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

http://www.wikidata.org/entity/Q35126030

description

2007 nî lūn-bûn

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2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2007 թվականի ապրիլին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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type

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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prefLabel

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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J.NEUROBIOLAGING.2007.02.029

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Neurobiology of Aging

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers.

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Diana Wu

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Eileen H Bigio

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Elizabeth Chen-Dodson

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Fernanda G De Felice

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Gene G Kinney

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Jasna Jerecic

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Mary P Lambert

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Pascale N Lacor

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Paul J Acton

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Paul J Shughrue

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P2860

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

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

Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity

PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations

Reversible memory loss in a mouse transgenic model of Alzheimer's disease

A specific amyloid-beta protein assembly in the brain impairs memory

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

Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins

Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse

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1334-1347

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9

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51385109

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17403556

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Alzheimer's disease

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3142933

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