N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. - Wikidata - awgldk - TriplyDB

N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits.

N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits.

http://www.wikidata.org/entity/Q37043304

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Calcium-Sensing Receptors of Human Neural Cells Play Crucial Roles in Alzheimer's Disease Alzheimer's disease--a panorama glimpse Neuronal seipin knockout facilitates Aβ-induced neuroinflammation and neurotoxicity via reduction of PPARγ in hippocampus of mouse Endothelial LRP1 transports amyloid-β(1-42) across the blood-brain barrier Numerical Simulations Reveal Randomness of Cu(II) Induced Aβ Peptide Dimerization under Conditions Present in Glutamatergic Synapses Focusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer's disease The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease Alzheimer therapy with an antibody against N-terminal Abeta 4-X and pyroglutamate Abeta 3-X.Amyloid-β Peptide Aβ3pE-42 Induces Lipid Peroxidation, Membrane Permeabilization, and Calcium Influx in Neurons.Sequence proximity between Cu(II) and Cu(I) binding sites of human copper transporter 1 model peptides defines reactivity with ascorbate and O2.Physical activity delays hippocampal neurodegeneration and rescues memory deficits in an Alzheimer disease mouse model N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody.Abundance of Aβ₅-x like immunoreactivity in transgenic 5XFAD, APP/PS1KI and 3xTG mice, sporadic and familial Alzheimer's disease.Deciphering the molecular profile of plaques, memory decline and neuron loss in two mouse models for Alzheimer's disease by deep sequencing.Truncated and modified amyloid-beta species.Amyloid-β as a biomarker for Alzheimer's disease: quantification methods in body fluids.Generation of aggregation prone N-terminally truncated amyloid β peptides by meprin β depends on the sequence specificity at the cleavage site.BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells.Phosphorylation Interferes with Maturation of Amyloid-β Fibrillar Structure in the N Terminus.Phosphorylation modifies the molecular stability of β-amyloid deposits.Isotope-edited FTIR reveals distinct aggregation and structural behaviors of unmodified and pyroglutamylated amyloid β peptides.The prion protein regulates beta-amyloid-mediated self-renewal of neural stem cells in vitro.Do astrocytes collaborate with neurons in spreading the "infectious" aβ and Tau drivers of Alzheimer's disease?N-truncated Aβ4-x peptides in sporadic Alzheimer's disease cases and transgenic Alzheimer mouse models.Amyloidogenicity and toxicity of the reverse and scrambled variants of amyloid-β 1-42 Aβ truncated species: Implications for brain clearance mechanisms and amyloid plaque deposition.Structural and functional analyses of pyroglutamate-amyloid-β-specific antibodies as a basis for Alzheimer immunotherapy.Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury.Unmodified and pyroglutamylated amyloid β peptides form hypertoxic hetero-oligomers of unique secondary structure.N-truncated Aβ2-X starting with position two in sporadic Alzheimer's disease cases and two Alzheimer mouse models.Stereological estimation of neuron number and plaque load in the hippocampal region of a transgenic rat model of Alzheimer's disease.The role of astrocytes in amyloid production and Alzheimer's disease.Super-Resolution Microscopy of Cerebrospinal Fluid Biomarkers as a Tool for Alzheimer's Disease Diagnostics.Expression of the Alzheimer's Disease Mutations AβPP695sw and PSEN1M146I in Double-Transgenic Göttingen Minipigs.Dose-Dependent Neuroprotection and Neurotoxicity of Simvastatin through Reduction of Farnesyl Pyrophosphate in Mice Treated with Intracerebroventricular Injection of Aβ 1-42.A Functional Role for Aβ in Metal Homeostasis? N-Truncation and High-Affinity Copper Binding.New Thymoquinol Glycosides and Neuroprotective Dibenzocyclooctane Lignans from the Rattan Stems of Schisandra chinensis.Synergistic Effect on Neurodegeneration by N-Truncated Aβ4-42 and Pyroglutamate Aβ3-42 in a Mouse Model of Alzheimer's Disease.Comprehensive Characterization of the Pyroglutamate Amyloid-β Induced Motor Neurodegenerative Phenotype of TBA2.1 Mice.Binding Modes of Phthalocyanines to Amyloid β Peptide and Their Effects on Amyloid Fibril Formation.

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N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits.

http://www.wikidata.org/entity/Q37043304

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

@tr

scientific article published on 18 May 2013

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

N-truncated amyloid β (Aβ) 4-4 ...... g-lasting behavioral deficits.

@en

N-truncated amyloid β

@nl

type

label

N-truncated amyloid β (Aβ) 4-4 ...... g-lasting behavioral deficits.

@en

N-truncated amyloid β

@nl

prefLabel

N-truncated amyloid β (Aβ) 4-4 ...... g-lasting behavioral deficits.

@en

N-truncated amyloid β

@nl

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S00401-013-1129-2

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Acta Neuropathologica

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N-truncated amyloid β (Aβ) 4-4 ...... g-lasting behavioral deficits.

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Frederick Sprenger

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Jessica L Wittnam

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Katharina Dietrich

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Oliver Wirths

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Sophie Papot-Couturier

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Thierry Pillot

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Thomas A Bayer

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Thomas Lefebvre

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Yvonne Bouter

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P2860

Extracellular phosphorylation of the amyloid β-peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease.

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Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease

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

Alzheimer's disease: genes, proteins, and therapy

Morris water maze: procedures for assessing spatial and related forms of learning and memory

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

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

Relative expression software tool (REST©) for group-wise comparison and statistical analysis of relative expression results in real-time PCR

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s00401-013-1129-2

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scholarly article

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10.1007/S00401-013-1129-2

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2

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126

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Markus Zweckstetter

Nasrollah Rezaei-Ghaleh

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2013-05-18T00:00:00Z

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236920289

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