Neurofibrillary tangle formation by introducing wild-type human tau into APP transgenic mice. - Wikidata - awgldk - TriplyDB

Neurofibrillary tangle formation by introducing wild-type human tau into APP transgenic mice.

Neurofibrillary tangle formation by introducing wild-type human tau into APP transgenic mice.

http://www.wikidata.org/entity/Q50860536

about

Tau physiology and pathomechanisms in frontotemporal lobar degeneration Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities Discovery of 5-(4-hydroxyphenyl)-3-oxo-pentanoic acid [2-(5-methoxy-1H-indol-3-yl)-ethyl]-amide as a neuroprotectant for Alzheimer's disease by hybridization of curcumin and melatonin Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.Passive immunotherapy of tauopathy targeting pSer413-tau: a pilot study in mice.What we can learn from animal models about cerebral multi-morbidity.Barriers to developing a valid rodent model of Alzheimer's disease: from behavioral analysis to etiological mechanisms The domestic cat as a natural animal model of Alzheimer's disease.Human tau increases amyloid β plaque size but not amyloid β-mediated synapse loss in a novel mouse model of Alzheimer's disease.In vivo tracking of tau pathology using positron emission tomography (PET) molecular imaging in small animals.Conformation-specific antibodies to target amyloid β oligomers and their application to immunotherapy for Alzheimer's disease.Alzheimer's disease: experimental models and reality.Interactions of pathological proteins in neurodegenerative diseases.Rifampicin is a candidate preventive medicine against amyloid-β and tau oligomers.The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade.Untangling Tau and Iron: Exploring the Interaction Between Iron and Tau in Neurodegeneration

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P2860

Neurofibrillary tangle formation by introducing wild-type human tau into APP transgenic mice.

http://www.wikidata.org/entity/Q50860536

description

2014 nî lūn-bûn

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2014年の論文

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2014年学术文章

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2014年学术文章

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2014年学术文章

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2014年学术文章

@zh-my

2014年学术文章

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2014年學術文章

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2014年學術文章

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2014年學術文章

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name

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@en

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@nl

type

label

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@en

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@nl

prefLabel

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@en

Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@nl

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S00401-014-1259-1

P1433

Acta Neuropathologica

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Neurofibrillary tangle formati ...... tau into APP transgenic mice.

@en

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Akihiko Takashima

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

Hiroshi Mori

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Satomi Maekawa

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

Takami Tomiyama

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Tetsuya Kimura

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

Tomohiro Umeda

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

Interaction of tau with the neural membrane cortex is regulated by phosphorylation at sites that are modified in paired helical filaments

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

Interaction of tau with the neural plasma membrane mediated by tau's amino-terminal projection domain

Molecular cross talk between misfolded proteins in animal models of Alzheimer's and prion diseases

Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

Induction of tau pathology by intracerebral infusion of amyloid-beta -containing brain extract and by amyloid-beta deposition in APP x Tau transgenic mice

Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models

Age-dependent induction of congophilic neurofibrillary tau inclusions in tau transgenic mice

Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway

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s00401-014-1259-1

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685-698

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scholarly article

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10.1007/S00401-014-1259-1

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5

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127

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2014-02-15T00:00:00Z

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24531886

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