Early and selective impairments in axonal transport kinetics of synaptic cargoes induced by soluble amyloid β-protein oligomers.
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Diabetes Mellitus Induces Alzheimer's Disease Pathology: Histopathological Evidence from Animal ModelsA dynamic formin-dependent deep F-actin network in axons.Amyloid-Beta Induced Changes in Vesicular Transport of BDNF in Hippocampal NeuronsHuman A53T α-synuclein causes reversible deficits in mitochondrial function and dynamics in primary mouse cortical neuronsAmyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neuronsAlzheimer amyloid beta inhibition of Eg5/kinesin 5 reduces neurotrophin and/or transmitter receptor function.Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β.Active zone proteins are transported via distinct mechanisms regulated by Par-1 kinase.Visualizing APP and BACE-1 approximation in neurons yields insight into the amyloidogenic pathway.Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer's disease.Fast vesicle transport is required for the slow axonal transport of synapsinInteraction of membrane/lipid rafts with the cytoskeleton: impact on signaling and function: membrane/lipid rafts, mediators of cytoskeletal arrangement and cell signaling.Impaired retrograde transport of axonal autophagosomes contributes to autophagic stress in Alzheimer's disease neurons.The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer's disease.Axonal degeneration in Alzheimer's disease: when signaling abnormalities meet the axonal transport system.The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.Amyloid-β Peptide Is Needed for cGMP-Induced Long-Term Potentiation and Memory.Alzheimer's disease-related amyloid-β induces synaptotoxicity in human iPS cell-derived neurons.Intracellular amyloid β oligomers impair organelle transport and induce dendritic spine loss in primary neurons.Defective lysosomal proteolysis and axonal transport are early pathogenic events that worsen with age leading to increased APP metabolism and synaptic Abeta in transgenic APP/PS1 hippocampus.Activity-induced convergence of APP and BACE-1 in acidic microdomains via an endocytosis-dependent pathway.Prion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.The physical approximation of APP and BACE-1: A key event in alzheimer's disease pathogenesis.Mutant spastin proteins promote deficits in axonal transport through an isoform-specific mechanism involving casein kinase 2 activation.
P2860
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P2860
Early and selective impairments in axonal transport kinetics of synaptic cargoes induced by soluble amyloid β-protein oligomers.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Early and selective impairment ...... e amyloid β-protein oligomers.
@en
type
label
Early and selective impairment ...... e amyloid β-protein oligomers.
@en
prefLabel
Early and selective impairment ...... e amyloid β-protein oligomers.
@en
P2093
P2860
P1433
P1476
Early and selective impairment ...... e amyloid β-protein oligomers.
@en
P2093
David A Scott
Edward H Koo
Kryslaine Radomski
Steven D Edland
Subhojit Roy
P2860
P304
P356
10.1111/J.1600-0854.2012.01340.X
P577
2012-02-27T00:00:00Z