Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence. - Wikidata - wikimedia - TriplyDB

Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence.

Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence.

http://www.wikidata.org/entity/Q35103366

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Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins Regulation of the Postsynaptic Compartment of Excitatory Synapses by the Actin Cytoskeleton in Health and Its Disruption in Disease Pathogenesis of synaptic degeneration in Alzheimer's disease and Lewy body disease The Beta-amyloid protein of Alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton Early-onset and robust amyloid pathology in a new homozygous mouse model of Alzheimer's disease Gain of BDNF Function in Engrafted Neural Stem Cells Promotes the Therapeutic Potential for Alzheimer's Disease.A new function for the fragile X mental retardation protein in regulation of PSD-95 mRNA stability Hsp90 chaperone inhibitor 17-AAG attenuates Aβ-induced synaptic toxicity and memory impairment Synaptic protein α1-takusan mitigates amyloid-β-induced synaptic loss via interaction with tau and postsynaptic density-95 at postsynaptic sites Tau-mediated synaptic damage in Alzheimer's disease Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline Transcriptome analysis of synaptoneurosomes identifies neuroplasticity genes overexpressed in incipient Alzheimer's disease.Omega-3 fatty acids and dementia.Molecular mechanisms of neurodegeneration in Alzheimer's disease.Early calcium dysregulation in Alzheimer's disease: setting the stage for synaptic dysfunction.Flow cytometry analysis of synaptosomes from post-mortem human brain reveals changes specific to Lewy body and Alzheimer's disease.Is synaptic loss a unique hallmark of Alzheimer's disease?Amyloid-beta protein oligomer at low nanomolar concentrations activates microglia and induces microglial neurotoxicity.Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease.Microglial P2X₇ receptor expression is accompanied by neuronal damage in the cerebral cortex of the APPswe/PS1dE9 mouse model of Alzheimer's disease.N-cadherin regulates p38 MAPK signaling via association with JNK-associated leucine zipper protein: implications for neurodegeneration in Alzheimer disease Drosophila models of neurodegenerative diseases.Synaptic changes in the dentate gyrus of APP/PS1 transgenic mice revealed by electron microscopy.Dendritic spine dynamics--a key role for kalirin-7.Phospho-dependent ubiquitination and degradation of PAR-1 regulates synaptic morphology and tau-mediated Aβ toxicity in Drosophila.Detection of peri-synaptic amyloid-β pyroglutamate aggregates in early stages of Alzheimer's disease and in AβPP transgenic mice using a novel monoclonal antibody Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease.Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold.AD synapses contain abundant Aβ monomer and multiple soluble oligomers, including a 56-kDa assembly Pre-synaptic C-terminal truncated tau is released from cortical synapses in Alzheimer's disease A critical role for the PAR-1/MARK-tau axis in mediating the toxic effects of Aβ on synapses and dendritic spines Synapses and dendritic spines as pathogenic targets in Alzheimer's disease.Isolation of synaptic terminals from Alzheimer's disease cortex Preferential accumulation of amyloid-beta in presynaptic glutamatergic terminals (VGluT1 and VGluT2) in Alzheimer's disease cortex.Staying connected: synapses in Alzheimer disease.Apolipoprotein E level and cholesterol are associated with reduced synaptic amyloid beta in Alzheimer's disease and apoE TR mouse cortex Extensive p-tau pathology and SDS-stable p-tau oligomers in Alzheimer's cortical synapses.Early presynaptic and postsynaptic calcium signaling abnormalities mask underlying synaptic depression in presymptomatic Alzheimer's disease mice.Proteogenomics of synaptosomal mitochondrial oxidative stress.Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer's disease

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Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence.

http://www.wikidata.org/entity/Q35103366

description

2004 nî lūn-bûn

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2004 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2004 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年论文

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name

Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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The American Journal of Pathology

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Synaptic changes in Alzheimer' ...... decreased PSD-95 fluorescence.

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Carol A Miller

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

Dorothy J Wiley

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Fusheng Yang

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Gregory M Cole

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Jeffrey A Fein

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Karen Hoppens Gylys

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P2860

Drebrin, a dendritic spine protein, is manifold decreased in brains of patients with Alzheimer's disease and Down syndrome

Amyloid beta peptide load is correlated with increased beta-secretase activity in sporadic Alzheimer's disease patients

Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Domain interaction between NMDA receptor subunits and the postsynaptic density protein PSD-95

Disappearance of actin-binding protein, drebrin, from hippocampal synapses in Alzheimer's disease

Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment

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

Alzheimer's disease is a synaptic failure

High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation

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Alzheimer's disease

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1618663

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