The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease. - Wikidata - wikimedia - TriplyDB

The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

http://www.wikidata.org/entity/Q38400601

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The Role of MAPT in Neurodegenerative Diseases: Genetics, Mechanisms and Therapy Structure of Crenezumab Complex with Aβ Shows Loss of β-Hairpin.Targeting β-amyloid plaques and oligomers: development of near-IR fluorescence imaging probes.A Mitocentric View of Alzheimer's Disease.The Role of ADAM10 in Alzheimer's Disease.Aβ Peptide Originated from Platelets Promises New Strategy in Anti-Alzheimer's Drug Development.Ebselen ameliorates β-amyloid pathology, tau pathology, and cognitive impairment in triple-transgenic Alzheimer's disease mice.Involvement of Astrocytes in Alzheimer's Disease from a Neuroinflammatory and Oxidative Stress Perspective.Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer's Disease.ABBY: A phase 2 randomized trial of crenezumab in mild to moderate Alzheimer disease.Effects and mechanism of amyloid β1-42 on mitochondria in astrocytes.Amyloid β peptides are differentially vulnerable to preanalytical surface exposure, an effect incompletely mitigated by the use of ratios.APP21 transgenic rats develop age-dependent cognitive impairment and microglia accumulation within white matter tracts

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The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

http://www.wikidata.org/entity/Q38400601

description

2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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name

The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

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The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

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The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

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Molecular Neurobiology

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The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.

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Jinyuan Liu

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Zi-Xuan Wang

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P2860

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers

Long-Term Potentiation and Memory

Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer's disease

Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein

Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism

Synthetic amyloid-beta oligomers impair long-term memory independently of cellular prion protein

Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments.

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

mTOR signaling: at the crossroads of plasticity, memory and disease

Aggregation and disaggregation of senile plaques in Alzheimer disease

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Alzheimer's disease