Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta - Wikidata - thesis-toulmin - TriplyDB

Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta

Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta

http://www.wikidata.org/entity/Q28239322

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown Effects of ALS-related SOD1 mutants on dynein- and KIF5-mediated retrograde and anterograde axonal transport Protein phosphatase 5 protects neurons against amyloid-beta toxicity The toxicity of amyloid β oligomers Alterations in Mitochondrial Quality Control in Alzheimer's Disease TDP-43: a new player on the AD field?The axonal transport of mitochondria Amyloid beta: multiple mechanisms of toxicity and only some protective effects?Amyloid β precursor protein as a molecular target for amyloid β--induced neuronal degeneration in Alzheimer's disease Axonal transport of APP and the spatial regulation of APP cleavage and function in neuronal cells Defects in mitochondrial dynamics and metabolomic signatures of evolving energetic stress in mouse models of familial Alzheimer's disease The Emerging Roles of the Calcineurin-Nuclear Factor of Activated T-Lymphocytes Pathway in Nervous System Functions and Diseases Synaptic transmission block by presynaptic injection of oligomeric amyloid beta Tau reduction prevents Abeta-induced defects in axonal transport.Quantitative in vivo measurement of early axonal transport deficits in a triple transgenic mouse model of Alzheimer's disease using manganese-enhanced MRI Animal models for Alzheimer's disease and frontotemporal dementia: a perspective Mechanisms of U87 astrocytoma cell uptake and trafficking of monomeric versus protofibril Alzheimer's disease amyloid-β proteins Phosphorylation in the amino terminus of tau prevents inhibition of anterograde axonal transport.Amyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neurons Loss of c-Jun N-terminal kinase-interacting protein-1 does not affect axonal transport of the amyloid precursor protein or Aβ production.Complex environment experience rescues impaired neurogenesis, enhances synaptic plasticity, and attenuates neuropathology in familial Alzheimer's disease-linked APPswe/PS1DeltaE9 mice.Accumulation of intraneuronal Abeta correlates with ApoE4 genotype Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation.Neuroproteomics approaches to decipher neuronal regeneration and degeneration.Abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease.Neuronal and axonal loss are selectively linked to fibrillar amyloid-{beta} within plaques of the aged primate cerebral cortex.GSK3β is involved in the relief of mitochondria pausing in a Tau-dependent manner Protein kinases CK1 and CK2 as new targets for neurodegenerative diseases.Abnormal intracellular accumulation and extracellular Aβ deposition in idiopathic and Dup15q11.2-q13 autism spectrum disorders Aberrant subcellular neuronal calcium regulation in aging and Alzheimer's disease Cyclophilin D deficiency rescues axonal mitochondrial transport in Alzheimer's neurons Amyloid beta impairs mitochondrial anterograde transport and degenerates synapses in Alzheimer's disease neurons.Isolating toxic insulin amyloid reactive species that lack β-sheets and have wide pH stability Fiber Tracts Anomalies in APPxPS1 Transgenic Mice Modeling Alzheimer's Disease.Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's disease Contractile dysfunction in muscle may underlie androgen-dependent motor dysfunction in spinal bulbar muscular atrophy.The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer's disease.AD synapses contain abundant Aβ monomer and multiple soluble oligomers, including a 56-kDa assembly ENU mutagenesis screen to establish motor phenotypes in wild-type mice and modifiers of a pre-existing motor phenotype in tau mutant mice.The Organization of Mitochondrial Quality Control and Life Cycle in the Nervous System In Vivo in the Absence of PINK1.

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P2860

Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta

http://www.wikidata.org/entity/Q28239322

description

2009 nî lūn-bûn

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2009 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2009 թվականի ապրիլին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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type

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

@nl

prefLabel

Disruption of fast axonal tran ...... for intraneuronal amyloid beta

@ast

Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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PNAS.0901229106

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

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Disruption of fast axonal tran ...... for intraneuronal amyloid beta

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P2093

A Deshpande

http://www.w3.org/2001/XMLSchema#string

C Yu

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G Morfini

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G Pigino

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J Busciglio

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M LaDu

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S Brady

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Y Atagi

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P2860

A Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease

A kinesin heavy chain (KIF5A) mutation in hereditary spastic paraplegia (SPG10)

Synaptic transmission block by presynaptic injection of oligomeric amyloid beta

Alzheimer's presenilin 1 mutations impair kinesin-based axonal transport

Ca2+-dependent dephosphorylation of kinesin heavy chain on beta-granules in pancreatic beta-cells. Implications for regulated beta-granule transport and insulin exocytosis

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

Alzheimer's disease: the amyloid cascade hypothesis

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

Alzheimer's disease is a synaptic failure

Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function

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19321417

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