Neuronal Expression of Truncated Tau Efficiently Promotes Neurodegeneration in Animal Models: Pitfalls of Toxic Oligomer Analysis

No abstract is available for this paper.

• Publication year

  2017

• Venue

  Journal of Alzheimer's Disease

• Publication date

  2017-05-17

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.3233/JAD-161124PMID 28527208
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Co-expression of truncated and full-length tau induces severe neurotoxicity

  2016cited by this paper
• The neuritic plaque facilitates pathological conversion of tau in an Alzheimer's disease mouse model

  2016cited by this paper
• Caspase-cleaved tau exhibits rapid memory impairment associated with tau oligomers in a transgenic mouse model.

  2016cited by this paper
• Human Truncated Tau Induces Mature Neurofibrillary Pathology in a Mouse Model of Human Tauopathy

  2016influential reference
• Calpain Activation in Alzheimer's Model Mice Is an Artifact of APP and Presenilin Overexpression

  2016cited by this paper
• Tauopathy induced by low level expression of a human brain-derived tau fragment in mice is rescued by phenylbutyrate

  2016influential reference
• SDS-PAGE analysis of Aβ oligomers is disserving research into Alzheimer´s disease: appealing for ESI-IM-MS

  2015cited by this paper
• Truncated tau deregulates synaptic markers in rat model for human tauopathy

  2015influential reference
• Role of the Tau N-terminal region in microtubule stabilization revealed by new endogenous truncated forms

  2015cited by this paper
• Intraneuronal accumulation of misfolded tau protein induces overexpression of Hsp27 in activated astrocytes.

  2015cited by this paper
• Different pathways of molecular pathophysiology underlie cognitive and motor tauopathy phenotypes in transgenic models for Alzheimer’s disease and frontotemporal lobar degeneration

  2014cited by this paper
• Oligomers, fact or artefact? SDS-PAGE induces dimerization of β-amyloid in human brain samples

  2013cited by this paper
• Tauopathies and Tau Oligomers

  2013cited by this paper
• Protein Truncation as a Common Denominator of Human Neurodegenerative Foldopathies

  2013cited by this paper
• Formation and Propagation of Tau Oligomeric Seeds

  2013cited by this paper
• Regulatable transgenic mouse models of Alzheimer disease: onset, reversibility and spreading of Tau pathology

  2013influential reference
• Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature

  2012cited by this paper
• The self-perpetuating tau truncation circle.

  2012cited by this paper
• First transgenic rat model developing progressive cortical neurofibrillary tangles.

  2012influential reference
• Tau-Induced Defects in Synaptic Plasticity, Learning, and Memory Are Reversible in Transgenic Mice after Switching Off the Toxic Tau Mutant

  2011cited by this paper
• Truncation of tau at E391 Promotes Early Pathologic Changes in Transgenic Mice

  2011influential reference
• CSF phospho-tau correlates with behavioural decline and brain insoluble phospho-tau levels in a rat model of tauopathy

  2010cited by this paper
• Transition of Tau Protein from Disordered to Misordered in Alzheimer’s Disease

  2010cited by this paper
• Genetic background modifies neurodegeneration and neuroinflammation driven by misfolded human tau protein in rat model of tauopathy: implication for immunomodulatory approach to Alzheimer's disease

  2010influential reference
• Alzheimer disease: Caspases first

  2010cited by this paper
• NeuroScale, the battery of behavioral tests with novel scoring system for phenotyping of transgenic rat model of tauopathy.

  2009cited by this paper
• Misfolded tau protein and disease modifying pathways in transgenic rodent models of human tauopathies

  2009cited by this paper
• Preserving free thiols of intrinsically disordered tau protein without the use of a reducing agent.

  2008cited by this paper
• Detecting native folds in mixtures of proteins that contain disulfide bonds

  2008cited by this paper
• Truncated tau expression levels determine life span of a rat model of tauopathy without causing neuronal loss or correlating with terminal neurofibrillary tangle load

  2008cited by this paper
• The Potential for β-Structure in the Repeat Domain of Tau Protein Determines Aggregation, Synaptic Decay, Neuronal Loss, and Coassembly with Endogenous Tau in Inducible Mouse Models of Tauopathy

  2008cited by this paper
• Accumulation of Pathological Tau Species and Memory Loss in a Conditional Model of Tauopathy

  2007cited by this paper
• Neurodegeneration caused by expression of human truncated tau leads to progressive neurobehavioural impairment in transgenic rats.

  2007influential reference
• Intrinsically Disordered Proteins in the Neurodegenerative Processes: Formation of Tau Protein Paired Helical Filaments and Their Analysis

  2006cited by this paper
• Truncated tau from sporadic Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo

  2006cited by this paper
• Pathways for protein disulphide bond formation.

  2000cited by this paper
• Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein

  2000cited by this paper
• Glycoproteins form mixed disulphides with oxidoreductases during folding in living cells

  1999cited by this paper
• Determination of the Cysteine and Cystine Content of Proteins by Amino Acid Analysis: Application to the Characterization of Disulfide-Coupled Folding Intermediates

  1998cited by this paper
• Evolution of the neuropathology of Alzheimer's disease

  1996cited by this paper
• Oxidation of cysteine-322 in the repeat domain of microtubule-associated protein tau controls the in vitro assembly of paired helical filaments.

  1995cited by this paper
• Structural studies of tau protein and Alzheimer paired helical filaments show no evidence for beta-structure.

  1994cited by this paper
• Molecular characterization of the minimal protease resistant tau unit of the Alzheimer's disease paired helical filament.

  1993cited by this paper
• Isolation of a fragment of tau derived from the core of the paired helical filament of Alzheimer disease.

  1988cited by this paper

• Plasma Leptin Reflects Progression of Neurofibrillary Pathology in Animal Model of Tauopathy

  2020cites this paper
• Plasma Leptin Reflects Progression of Neurofibrillary Pathology in Animal Model of Tauopathy

  2020cites this paper
• MIRRAGGE – Minimum Information Required for Reproducible AGGregation Experiments

  2020cites this paper
• The cellular prion protein and its derived fragments in human prion diseases and their role as potential biomarkers

  2019cites this paper
• Structure and Functions of Microtubule Associated Proteins Tau and MAP2c: Similarities and Differences

  2019cites this paper
• Tau Conformation as a Target for Disease-Modifying Therapy: The Role of Truncation

  2018cites this paper
• AADvac1, an Active Immunotherapy for Alzheimer’s Disease and Non Alzheimer Tauopathies: An Overview of Preclinical and Clinical Development

  2018cites this paper
• Ten Years of Tau-Targeted Immunotherapy: The Path Walked and the Roads Ahead

  2018cites this paper