ArticleJournal of Alzheimer's disease : JAD2016
Halting of Caspase Activity Protects Tau from MC1-Conformational Change and Aggregation.
Article in Journal of Alzheimer's disease : JAD, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Tau aggregation induces cell death in iPSC-derived neurons.Aging brain · 2025Article
- JNK3 Overexpression in the Entorhinal Cortex Impacts on the Hippocampus and Induces Cognitive Deficiencies and Tau Misfolding.ACS chemical neuroscience · 2023Article
- Patterns of neuronal Rhes as a novel hallmark of tauopathies.Acta neuropathologica · 2021Article
- Small molecule modulation of the p75 neurotrophin receptor inhibits multiple amyloid beta-induced tau pathologies.Scientific reports · 2020Article
- Small-molecule modulation of the p75 neurotrophin receptor inhibits a wide range of tau molecular pathologies and their sequelae in P301S tauopathy mice.Acta neuropathologica communications · 2020Article
- Do Post-Translational Modifications Influence Protein Aggregation in Neurodegenerative Diseases: A Systematic Review.Brain sciences · 2020Review
- Tau protein aggregates inhibit the protein-folding and vesicular trafficking arms of the cellular proteostasis network.The Journal of biological chemistry · 2019Article
- A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy.Science translational medicine · 2019Article
- Modulation of Disordered Proteins with a Focus on Neurodegenerative Diseases and Other Pathologies.International journal of molecular sciences · 2019Review
- Chronic Sleep Disruption Advances the Temporal Progression of Tauopathy in P301S Mutant Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Active full-length DNA AβAlzheimer's research & therapy · 2018Article
- Tau Proteolysis in the Pathogenesis of Tauopathies: Neurotoxic Fragments and Novel Biomarkers.Journal of Alzheimer's disease : JAD · 2018Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Intracellular neurofibrillary tangles (NFTs) are the hallmark of Alzheimer's disease and other tauopathies in which tau, a microtubule-associated protein, loses its ability to stabilize microtubules. Several post-translational modifications including phosphorylation and truncation increase tau's propensity to aggregate thus forming NFTs; however, the mechanisms underlying tau conformational change and aggregation still remain to be defined. Caspase activation and subsequent proteolytic cleavage of tau is thought to be a potential trigger of this disease-related pathological conformation. The aim of this work was to investigate the link between caspase activation and a disease-related conformational change of tau in a neuroblastoma cell-based model of spontaneous tau aggregation. We demonstrated that caspase induction initiates proteolytic cleavage of tau and generation of conformationally altered and aggregated tau recognized by the MC1 conformational antibody. Most importantly, these events were shown to be attenuated with caspase inhibitors. This implies that therapeutics aimed at inhibiting caspase-mediated tau cleavage may prove beneficial in slowing cleavage and aggregation, thus potentially halting tau pathology and disease progression.
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Registered trials
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