ArticleHuman molecular genetics2020
Synergistic toxicity between tau and amyloid drives neuronal dysfunction and neurodegeneration in transgenic C. elegans.
Article in Human molecular genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 63 citations in OpenAlex.
- Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer's disease.Nature aging · 2021Trial
- Loss of endogenous tau suppresses APOE4-induced patterned behavioral decline and axon dysmorphia in a model of Alzheimer's disease.Disease models & mechanisms · 2026Article
- Iron toxicity potentiates cell-type specific amyloid beta proteotoxicity inbioRxiv : the preprint server for biology · 2026Article
- Dominant α-tubulin mutations rescue tauopathy neurodegenerative phenotypes inbioRxiv : the preprint server for biology · 2026Article
- Glutamatergic neuron degeneration inmicroPublication biology · 2026Article
- Tri-snRNP activity modulates tauopathy phenotypes.NAR molecular medicine · 2025Article
- Expression of polyglutamine repeats at the pathogenic threshold modestly enhances tau neurotoxicity and protein accumulation inmicroPublication biology · 2025Article
- Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025Review
- TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy.bioRxiv : the preprint server for biology · 2024Article
- Transgenic Dendra2::tau expression allows in vivo monitoring of tau proteostasis in Caenorhabditis elegans.Disease models & mechanisms · 2024Article
- Reevaluating tau reduction as a therapeutic approach for tauopathies: Insights and perspectives.Cytoskeleton (Hoboken, N.J.) · 2024Article
- Switching On/Off Amyloid Plaque Formation in Transgenic Animal Models of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Cytochrome P450 and Epoxide Hydrolase Metabolites in Aβ and tau-induced Neurodegeneration: Insights frombioRxiv : the preprint server for biology · 2023Article
- SPOP loss of function protects against tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Simple models to understand complex disease: 10 years of progress fromFrontiers in neuroscience · 2023Review
- TDP-43 promotes tau accumulation and selective neurotoxicity in bigenic Caenorhabditis elegans.Disease models & mechanisms · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- A sporadic Alzheimer's blood-brain barrier model for developing ultrasound-mediated delivery of Aducanumab and anti-Tau antibodies.Theranostics · 2022Article
- The Neuroepigenetic Landscape of Vertebrate and Invertebrate Models of Neurodegenerative Diseases.Epigenetics insights · 2022Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Aggregates of Aβ peptide and the microtubule-associated protein tau are key molecular hallmarks of Alzheimer's disease (AD). However, the interaction between these two pathologies and the mechanisms underlying disease progression have remained unclear. Numerous failed clinical trials suggest the necessity for greater mechanistic understanding in order to refine strategies for therapeutic discovery and development. To this end, we have generated a transgenic Caenorhabditis elegans model expressing both human Aβ1-42 peptide and human tau protein pan-neuronally. We observed exacerbated behavioral dysfunction and age-dependent neurodegenerative changes in the Aβ;tau transgenic animals. Further, these changes occurred in the Aβ;tau transgenic animals at greater levels than worms harboring either the Aβ1-42 or tau transgene alone and interestingly without changes to the levels of tau expression, phosphorylation or aggregation. Functional changes were partially rescued with the introduction of a genetic suppressor of tau pathology. Taken together, the data herein support a synergistic role for both Aβ and tau in driving neuronal dysfunction seen in AD. Additionally, we believe that the utilization of the genetically tractable C. elegans model will provide a key resource for dissecting mechanisms driving AD molecular pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.