ArticleJournal of neuropathology and experimental neurology2011
Truncation of tau at E391 promotes early pathologic changes in transgenic mice.
Article in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- dGAE(297-391) Tau Fragment Promotes Formation of Chronic Traumatic Encephalopathy-Like Tau Filaments.Angewandte Chemie (International ed. in English) · 2024Article
- Linking Diabetes to Alzheimer's Disease: Potential Roles of Glucose Metabolism and Alpha-Glucosidase.Current neuropharmacology · 2023Review
- Accumulation of C-terminal cleaved tau is distinctly associated with cognitive deficits, synaptic plasticity impairment, and neurodegeneration in aged mice.GeroScience · 2022Article
- Tau Seeding Mouse Models with Patient Brain-Derived Aggregates.International journal of molecular sciences · 2021Review
- Alzheimer's disease: phenotypic approaches using disease models and the targeting of tau protein.Expert opinion on therapeutic targets · 2020Review
- Impact of Tau on Neurovascular Pathology in Alzheimer's Disease.Frontiers in neurology · 2020Review
- Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration.Frontiers in neuroscience · 2018Review
- Amyloidogenesis of Tau protein.Protein science : a publication of the Protein Society · 2017Review
- Behind the curtain of tauopathy: a show of multiple players orchestrating tau toxicity.Cellular and molecular life sciences : CMLS · 2016Review
- Different pathways of molecular pathophysiology underlie cognitive and motor tauopathy phenotypes in transgenic models for Alzheimer's disease and frontotemporal lobar degeneration.Cellular and molecular life sciences : CMLS · 2015Article
- Specific calpain inhibition by calpastatin prevents tauopathy and neurodegeneration and restores normal lifespan in tau P301L mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Protein phosphorylation in neurodegeneration: friend or foe?Frontiers in molecular neuroscience · 2014Review
- Are tau aggregates toxic or protective in tauopathies?Frontiers in neurology · 2013Article
- Hyperglycemia-induced tau cleavage in vitro and in vivo: a possible link between diabetes and Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2013Article
- Structure and pathology of tau protein in Alzheimer disease.International journal of Alzheimer's disease · 2012Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Proteolytic cleavage of tau at glutamic acid 391 (E391) is linked to the pathogenesis of Alzheimer disease (AD). This C-terminal-truncated tau species exists in neurofibrillary tangles and abnormal neurites in the brains of AD patients and may potentiate tau polymerization. We generated a mouse model that expresses human tau truncated at E391 to begin to elucidate the role of this C-terminal-truncated tau species in the development of tau pathology. Our results show that truncated but otherwise wild-type human tau is sufficient to drive pretangle pathologic changes in tau, including accumulation of insoluble tau, somatodendritic redistribution, formation of pathologic conformations, and dual phosphorylation of tau at sites associated with AD pathology. In addition, these mice exhibit atypical neuritic tau immunoreactivity, including abnormal neuritic processes and dystrophic neurites. These results suggest that changes in tau proteolysis can initiate tauopathy.
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