Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
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β-hairpin-mediated formation of structurally distinct multimers of neurotoxic prion peptidesRationally designed turn promoting mutation in the amyloid-β peptide sequence stabilizes oligomers in solutionAccumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neuronsLarge aggregates are the major soluble Aβ species in AD brain fractionated with density gradient ultracentrifugationCystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease.Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.Opposite effects of low and high doses of Abeta42 on electrical network and neuronal excitability in the rat prefrontal cortex.Dendritic vulnerability in neurodegenerative disease: insights from analyses of cortical pyramidal neurons in transgenic mouse modelsInherent anti-amyloidogenic activity of human immunoglobulin gamma heavy chainsSensitive detection of Aβ protofibrils by proximity ligation--relevance for Alzheimer's diseaseContrasting disease and nondisease protein aggregation by molecular simulationβ-Amyloid inhibits E-S potentiation through suppression of cannabinoid receptor 1-dependent synaptic disinhibitionEffects of the English (H6R) and Tottori (D7N) familial Alzheimer disease mutations on amyloid beta-protein assembly and toxicity.A human monoclonal IgG that binds aβ assemblies and diverse amyloids exhibits anti-amyloid activities in vitro and in vivo.NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.Long-Term Potentiation at CA3-CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress.Interaction between prion protein and toxic amyloid β assemblies can be therapeutically targeted at multiple sitesDevelopment of beta-amyloid-induced neurodegeneration in Alzheimer's disease and novel neuroprotective strategies.Hereditary cerebral hemorrhage with amyloidosis-Dutch type.Familial Alzheimer's disease mutations differentially alter amyloid β-protein oligomerizationProtofibril assemblies of the arctic, Dutch, and Flemish mutants of the Alzheimer's Abeta1-40 peptideTransglutaminase induces protofibril-like amyloid beta-protein assemblies that are protease-resistant and inhibit long-term potentiationIncreased Number of Plasma B Cells Producing Autoantibodies Against Aβ42 Protofibrils in Alzheimer's Disease.Neurotransmitter receptor and time dependence of the synaptic plasticity disrupting actions of Alzheimer's disease Aβ in vivo.Amino acid position-specific contributions to amyloid beta-protein oligomerization.Tauroursodeoxycholic acid prevents E22Q Alzheimer's Abeta toxicity in human cerebral endothelial cells.The culprit behind amyloid beta peptide related neurotoxicity in Alzheimer's disease: oligomer size or conformation?Low-n oligomers as therapeutic targets of Alzheimer's disease.Alzheimer's disease, β-amyloid, glutamate, NMDA receptors and memantine--searching for the connectionsAlzheimer's disease Aβ assemblies mediating rapid disruption of synaptic plasticity and memory.Protective effects of testosterone on cognitive dysfunction in Alzheimer's disease model rats induced by oligomeric beta amyloid peptide 1-42.Sensitive ELISA detection of amyloid-beta protofibrils in biological samples.Acute intracerebral treatment with amyloid-beta (1-42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in freely behaving rats.CSF Biomarkers for Alzheimer's Disease Diagnosis.Novel rat Alzheimer's disease models based on AAV-mediated gene transfer to selectively increase hippocampal Abeta levels.Wnt-5a occludes Abeta oligomer-induced depression of glutamatergic transmission in hippocampal neurons.Application of Chitosan, Chitooligosaccharide, and Their Derivatives in the Treatment of Alzheimer's Disease.Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.Astroglial Responses to Amyloid-Beta Progression in a Mouse Model of Alzheimer's Disease.PTEN recruitment controls synaptic and cognitive function in Alzheimer's models.
P2860
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P2860
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh
2004年學術文章
@zh-hant
name
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@en
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@nl
type
label
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@en
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@nl
prefLabel
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@en
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@nl
P2093
P2860
P1476
Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo.
@en
P2093
Dennis J Selkoe
Dominic M Walsh
Igor Klyubin
Julia V Fadeeva
Roger Anwyl
William K Cullen
P2860
P304
P356
10.1111/J.1460-9568.2004.03389.X
P407
P577
2004-05-01T00:00:00Z