ArticleMolecular psychiatry2016
Co-expression of truncated and full-length tau induces severe neurotoxicity.
Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Selective white matter tract vulnerability associated with tau burden in progressive supranuclear palsy and Alzheimer's disease.European journal of nuclear medicine and molecular imaging · 2026Article
- Proteomic comparison of hippocampal neurofibrillary tangles in PART, intermediate Alzheimer's disease and advanced Alzheimer's disease.Acta neuropathologica · 2026Article
- Calbindin-D28k deficiency mediates tau-driven hippocampal hyperexcitement and cognitive impairment.Translational neurodegeneration · 2026Article
- N-terminally acetylated Met11-Tau: a new pathological truncated Tau species with functional relevance in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer's disease.Molecular psychiatry · 2025Article
- The Role and Pathogenesis of Tau Protein in Alzheimer's Disease.Biomolecules · 2025Review
- Autophagy-lysosomal-associated neuronal death in neurodegenerative disease.Acta neuropathologica · 2024Review
- Greater white matter degeneration and lower structural connectivity in non-amnestic vs. amnestic Alzheimer's disease.Frontiers in neuroscience · 2024Article
- "Prion-like" seeding and propagation of oligomeric protein assemblies in neurodegenerative disorders.Frontiers in neuroscience · 2024Review
- A novel transgenic mouse line with hippocampus-dominant and inducible expression of truncated human tau.Translational neurodegeneration · 2023Article
- Trans-seeding of Alzheimer-related tau protein by a yeast prion.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Article
- Retromer deficiency in Tauopathy models enhances the truncation and toxicity of Tau.Nature communications · 2022Article
- The prion-like transmission of tau oligomersFrontiers in aging neuroscience · 2022Review
- Non-Canonical Roles of Tau and Their Contribution to Synaptic Dysfunction.International journal of molecular sciences · 2021Review
- A new non-aggregative splicing isoform of human Tau is decreased in Alzheimer's disease.Acta neuropathologica · 2021Article
- Tau Seeding Mouse Models with Patient Brain-Derived Aggregates.International journal of molecular sciences · 2021Review
- Severe oligomeric tau toxicity can be reversed without long-term sequelae.Brain : a journal of neurology · 2021Article
- Caspase-6-cleaved Tau fails to induce Tau hyperphosphorylation and aggregation, neurodegeneration, glial inflammation, and cognitive deficits.Cell death & disease · 2021Article
- Critical Molecular and Cellular Contributors to Tau Pathology.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Abundant tau inclusions are a defining hallmark of several human neurodegenerative diseases, including Alzheimer's disease. Protein fragmentation is a widely observed event in neurodegenerative proteinopathies. The relevance of tau fragmentation for the neurodegenerative process in tauopathies has yet remained unclear. Here we found that co-expression of truncated and full-length human tau in mice provoked the formation of soluble high-molecular-weight tau, the failure of axonal transport, clumping of mitochondria, disruption of the Golgi apparatus and missorting of synaptic proteins. This was associated with extensive nerve cell dysfunction and severe paralysis by the age of 3 weeks. When the expression of truncated tau was halted, most mice recovered behaviorally and functionally. In contrast, co-expression of full-length tau isoforms did not result in paralysis. Truncated tau thus induces extensive but reversible neurotoxicity in the presence of full-length tau through the formation of nonfilamentous high-molecular-weight tau aggregates, in the absence of tau filaments. Targeting tau fragmentation may provide a novel approach for the treatment of human tauopathies.
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