Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation. - Wikidata - awgldk - TriplyDB

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

http://www.wikidata.org/entity/Q37061979

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Metals and Neuronal Metal Binding Proteins Implicated in Alzheimer's Disease Metallothionein and stress combine to affect multiple organ systems Peripheral delivery of a CNS targeted, metalo-protease reduces aβ toxicity in a mouse model of Alzheimer's disease Issues raised involving the copper hypotheses in the causation of Alzheimer's disease Divalent Copper as a Major Triggering Agent in Alzheimer's Disease Conditional knockout of the Menkes disease copper transporter demonstrates its critical role in embryogenesis Copper chelator induced efficient episodic memory recovery in a non-transgenic Alzheimer's mouse model Copper promotes the trafficking of the amyloid precursor protein Modulation of tau phosphorylation by environmental copper.Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes.Control of Alzheimer's amyloid beta toxicity by the high molecular weight immunophilin FKBP52 and copper homeostasis in Drosophila Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder Oral zinc reduces amyloid burden in Tg2576 mice Copper complexation screen reveals compounds with potent antibiotic properties against methicillin-resistant Staphylococcus aureus.A copper-lowering strategy attenuates amyloid pathology in a transgenic mouse model of Alzheimer's disease.Effects of a copper-deficient diet on the biochemistry, neural morphology and behavior of aged mice.CD36 upregulation mediated by intranasal LV-NRF2 treatment mitigates hypoxia-induced progression of Alzheimer's-like pathogenesis.Oligomers, fact or artefact? SDS-PAGE induces dimerization of β-amyloid in human brain samples.Cellular up-regulation of Nedd4 family interacting protein 1 (Ndfip1) using low levels of bioactive cobalt complexes.Alzheimer's disease and metals: a review of the involvement of cellular membrane receptors in metallosignalling.Alzheimer's disease & metals: therapeutic opportunities.Interactions between Aβ and mutated Tau lead to polymorphism and induce aggregation of Aβ-mutated tau oligomeric complexes GSK-3 in Neurodegenerative Diseases.Ferritin overexpression in Drosophila glia leads to iron deposition in the optic lobes and late-onset behavioral defects.Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation.Spin hamiltonian parameters for Cu(II)-prion peptide complexes from L-band electron paramagnetic resonance spectroscopy Copper modulation as a therapy for Alzheimer's disease?Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity Pharmacological activity of metal binding agents that alter copper bioavailability.An impaired mitochondrial electron transport chain increases retention of the hypoxia imaging agent diacetylbis(4-methylthiosemicarbazonato)copperII.Links between copper and cholesterol in Alzheimer's disease.Deletion of the type-1 interferon receptor in APPSWE/PS1ΔE9 mice preserves cognitive function and alters glial phenotype Neuroinflammation and copper in Alzheimer's disease.The Inorganic Side of NGF: Copper(II) and Zinc(II) Affect the NGF Mimicking Signaling of the N-Terminus Peptides Encompassing the Recognition Domain of TrkA Receptor.Copper complexes of bis(thiosemicarbazones): from chemotherapeutics to diagnostic and therapeutic radiopharmaceuticals.Metal attenuating therapies in neurodegenerative disease.Copper complexes as therapeutic agents.Modulating metals as a therapeutic strategy for Alzheimer's disease.Biochemistry of amyloid β-protein and amyloid deposits in Alzheimer disease.Metallostasis and amyloid β-degrading enzymes.

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P2860

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

http://www.wikidata.org/entity/Q37061979

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 02 January 2009

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@en

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@nl

type

label

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@en

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@nl

prefLabel

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@en

Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

@nl

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PNAS.0809057106

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Proceedings of the National Academy of Sciences of the United States of America

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Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.

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Aphrodite Caragounis

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Gulay Filiz

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Katrina Laughton

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Kevin J Barnham

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Keyla A Perez

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Lin Wai Hung

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Mikhalina Cortes

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Milawaty Nurjono

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Paul A Adlard

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Paul S Donnelly

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P2860

Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE

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

Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior

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

Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model

Tau-mediated neurodegeneration in Alzheimer's disease and related disorders

Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo.

Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice.

Glycogen synthase kinase-3 from rabbit skeletal muscle. Separation from cyclic-AMP-dependent protein kinase and phosphorylase kinase.

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381-386

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scholarly article

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10.1073/PNAS.0809057106

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2

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106

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Colin L. Masters

Anthony R. White

Irene Volitakis

Peter J. Crouch

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2009-01-02T00:00:00Z

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23719829

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19122148

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phosphorylation

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2626711

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