Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold. - Wikidata - wikimedia - TriplyDB

Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold.

Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold.

http://www.wikidata.org/entity/Q35290019

about

Metals and Neuronal Metal Binding Proteins Implicated in Alzheimer's Disease Shank3 is localized in axons and presynaptic specializations of developing hippocampal neurons and involved in the modulation of NMDA receptor levels at axon terminals The zinc dyshomeostasis hypothesis of Alzheimer's disease Phenotypic and functional analysis of SHANK3 stop mutations identified in individuals with ASD and/or ID.The Shank3 Interaction Partner ProSAPiP1 Regulates Postsynaptic SPAR Levels and the Maturation of Dendritic Spines in Hippocampal Neurons.Spatial memory deficits in a mouse model of late-onset Alzheimer's disease are caused by zinc supplementation and correlate with amyloid-beta levels Absence of amyloid β oligomers at the postsynapse and regulated synaptic Zn2+ in cognitively intact aged individuals with Alzheimer's disease neuropathology.Zinc and the aging brain FUS Mislocalization and Vulnerability to DNA Damage in ALS Patients Derived hiPSCs and Aging Motoneurons.Characterization of biometal profiles in neurological disorders.Biological metals and metal-targeting compounds in major neurodegenerative diseases.Relationship between Zinc (Zn (2+) ) and Glutamate Receptors in the Processes Underlying Neurodegeneration.Anatomy and Cell Biology of Autism Spectrum Disorder: Lessons from Human Genetics.Analysis of Genomewide DNA Methylation Reveals Differences in DNA Methylation Levels between Dormant and Naturally as well as Artificially Potentiated Pedicle Periosteum of Sika Deer (Cervus nippon).The role of postsynaptic density proteins in neural degeneration and regeneration.Zinc deficiency dysregulates the synaptic ProSAP/Shank scaffold and might contribute to autism spectrum disorders.Zinc Binding to S100B Affords Regulation of Trace Metal Homeostasis and Excitotoxicity in the Brain.Phosphoproteome analysis of an early onset mouse model (TgCRND8) of Alzheimer's disease reveals temporal changes in neuronal and glia signaling pathways.Effects of curcumin on synapses in APPswe/PS1dE9 mice.

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P2860

Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold.

http://www.wikidata.org/entity/Q35290019

description

2011 nî lūn-bûn

@nan

2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Amyloid beta protein-induced z ...... f the ProSAP2/Shank3 scaffold.

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Amyloid beta protein-induced z ...... f the ProSAP2/Shank3 scaffold.

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Amyloid beta protein-induced z ...... f the ProSAP2/Shank3 scaffold.

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Amyloid beta protein-induced z ...... f the ProSAP2/Shank3 scaffold.

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Molecular Neurodegeneration

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Amyloid beta protein-induced z ...... f the ProSAP2/Shank3 scaffold.

@en

P2093

Craig C Garner

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

Katrin I Andreasson

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Magali Arons

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Michael J Schmeisser

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Michael Schoen

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

Patrick R Hof

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

Patrick T Udvardi

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

Tobias M Boeckers

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

P2860

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

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

Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders

De novo mutations in the gene encoding the synaptic scaffolding protein SHANK3 in patients ascertained for schizophrenia.

Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior

Contribution of SHANK3 mutations to autism spectrum disorder

Elimination of zinc from synaptic vesicles in the intact mouse brain by disruption of the ZnT3 gene

Proline-rich synapse-associated protein-1/cortactin binding protein 1 (ProSAP1/CortBP1) is a PDZ-domain protein highly enriched in the postsynaptic density

Histochemically-reactive zinc in amyloid plaques, angiopathy, and degenerating neurons of Alzheimer's diseased brains

An architectural framework that may lie at the core of the postsynaptic density

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65

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scholarly article

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10.1186/1750-1326-6-65

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6

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Joseph D. Buxbaum

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Nathaniel S Woodling

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2011-09-22T00:00:00Z

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51663051

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21939532

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3189132

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