Synaptic defects associated with s-inclusion body myositis are prevented by copper.

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The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.Micromolar copper modifies electrical properties and spontaneous discharges of nodose ganglion neurons in vitro.

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Synaptic defects associated with s-inclusion body myositis are prevented by copper.

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http://www.wikidata.org/entity/Q54097741

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@en

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@nl

type

Item

label

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@en

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@nl

prefLabel

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@en

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@nl

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Synaptic defects associated with s-inclusion body myositis are prevented by copper.

@en

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N C Inestrosa

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R Aldunate

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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

beta-Amyloid(1-42) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer's disease pathology

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

Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine.

Alzheimer's disease is a synaptic failure

Intracellular amyloid-beta in Alzheimer's disease

Intracellular amyloid formation in muscle cells of Abeta-transgenic Caenorhabditis elegans: determinants and physiological role in copper detoxification.

Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34.

The Caenorhabditis elegans A beta 1-42 model of Alzheimer disease predominantly expresses A beta 3-42.

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection.

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s10534-012-9553-7

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scholarly article

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10.1007/S10534-012-9553-7

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2012-05-10T00:00:00Z

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224933143

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Synaptic defects associated with s-inclusion body myositis are prevented by copper.

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P2860

P2860

Synaptic defects associated with s-inclusion body myositis are prevented by copper.

description

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P1433

P1476

P2093

P2860

P2888

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P356

P433

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P5875

P698

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P1476

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P2888

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P577

P5875

P698