Tau acts as a mediator for Alzheimer's disease-related synaptic deficits. - Wikidata - wikimedia - TriplyDB

Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

http://www.wikidata.org/entity/Q38203031

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Altered protein phosphatase 2A methylation and Tau phosphorylation in the young and aged brain of methylenetetrahydrofolate reductase (MTHFR) deficient mice.Intraneuronal APP and extracellular Aβ independently cause dendritic spine pathology in transgenic mouse models of Alzheimer's disease.Nicotinic Acetylcholine Receptors Sensitize a MAPK-linked Toxicity Pathway on Prolonged Exposure to β-Amyloid.Opposite Neural Trajectories of Apolipoprotein E ϵ4 and ϵ2 Alleles with Aging Associated with Different Risks of Alzheimer's Disease.Regional tau deposition measured by [(18)F]THK5317 positron emission tomography is associated to cognition via glucose metabolism in Alzheimer's disease Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer's disease.ATF4: a Novel Potential Therapeutic Target for Alzheimer's Disease.The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.Intracellular amyloid β oligomers impair organelle transport and induce dendritic spine loss in primary neurons.Genetic influences on cognition in progressive supranuclear palsy.

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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

http://www.wikidata.org/entity/Q38203031

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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

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European Journal of Neuroscience

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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits

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P2093

Dezhi Liao

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Eric C Miller

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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

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

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

Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

Tau-aggregation inhibitor therapy for Alzheimer's disease

Stimulatory effect of α-synuclein on the tau-phosphorylation by GSK-3β

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

Amyloid-β oligomers induce synaptic damage via Tau-dependent microtubule severing by TTLL6 and spastin

Amyloid plaque core protein in Alzheimer disease and Down syndrome

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1202-1213

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scholarly article

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10.1111/EJN.12504

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7

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39

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Peter J Teravskis

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2014-04-01T00:00:00Z

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24712999

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Alzheimer's disease

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3983570

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