Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles. - Wikidata - wikimedia - TriplyDB

Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles.

Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles.

http://www.wikidata.org/entity/Q46332461

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Immunotherapy as treatment for Alzheimer’s disease Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism Immunization with amyloid-beta attenuates inclusion body myositis-like myopathology and motor impairment in a transgenic mouse model Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments.Methylene blue reduces aβ levels and rescues early cognitive deficit by increasing proteasome activity Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau Hyperphosphorylation of microtubule-associated protein tau: a promising therapeutic target for Alzheimer disease Active and passive immunotherapy for neurodegenerative disorders The Metamorphic Nature of the Tau Protein: Dynamic Flexibility Comes at a Cost Tau Oligomers: The Toxic Player at Synapses in Alzheimer's Disease Neuroimaging assessment of early and late neurobiological sequelae of traumatic brain injury: implications for CTE Chaperones in Neurodegeneration Alzheimer's therapeutics: translation of preclinical science to clinical drug development Tau-targeted treatment strategies in Alzheimer's disease Administration of a selective β2 adrenergic receptor antagonist exacerbates neuropathology and cognitive deficits in a mouse model of Alzheimer's disease Structural Correlates of Antibodies Associated with Acute Reversal of Amyloid -related Behavioral Deficits in a Mouse Model of Alzheimer Disease Spines, plasticity, and cognition in Alzheimer's model mice The ubiquitin-proteasome system in Alzheimer's disease Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation Ferulic acid is a nutraceutical β-secretase modulator that improves behavioral impairment and alzheimer-like pathology in transgenic mice A humanin derivative reduces amyloid beta accumulation and ameliorates memory deficit in triple transgenic mice Animal models for Alzheimer's disease and frontotemporal dementia: a perspective Zebrafish models of Tauopathy The KATP channel activator diazoxide ameliorates amyloid-β and tau pathologies and improves memory in the 3xTgAD mouse model of Alzheimer's disease.Alzheimer disease models and human neuropathology: similarities and differences Brain amyloid-β oligomers in ageing and Alzheimer's disease.mTOR regulates tau phosphorylation and degradation: implications for Alzheimer's disease and other tauopathies.R-flurbiprofen improves tau, but not Aß pathology in a triple transgenic model of Alzheimer's disease.Reducing AD-like pathology in 3xTg-AD mouse model by DNA epitope vaccine - a novel immunotherapeutic strategy.Detection of increased scyllo-inositol in brain with magnetic resonance spectroscopy after dietary supplementation in Alzheimer's disease mouse models.Identification of oligomers at early stages of tau aggregation in Alzheimer's disease.Expression of neprilysin in skeletal muscle reduces amyloid burden in a transgenic mouse model of Alzheimer disease Blocking IL-1 signaling rescues cognition, attenuates tau pathology, and restores neuronal β-catenin pathway function in an Alzheimer's disease model.Genetically altering Abeta distribution from the brain to the vasculature ameliorates tau pathology Genetic suppression of β2-adrenergic receptors ameliorates tau pathology in a mouse model of tauopathies.Effects of dietary supplementation of carnosine on mitochondrial dysfunction, amyloid pathology, and cognitive deficits in 3xTg-AD mice.Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylation.Mechanisms of tau-induced neurodegeneration.RTN/Nogo in forming Alzheimer's neuritic plaques.Systemic vaccination with anti-oligomeric monoclonal antibodies improves cognitive function by reducing Aβ deposition and tau pathology in 3xTg-AD mice

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P2860

Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles.

http://www.wikidata.org/entity/Q46332461

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2006 nî lūn-bûn

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Reduction of soluble Abeta and ...... mice with plaques and tangles.

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Antonella Caccamo

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David H Cribbs

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Frank M LaFerla

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Masashi Kitazawa

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Salvatore Oddo

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Vitaly Vasilevko

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P2860

Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

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

Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Abeta and synaptic dysfunction

Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function

Tau suppression in a neurodegenerative mouse model improves memory function

Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse

A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.

Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease.

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