ArticleNeurobiology of disease2022
FTD-associated mutations in Tau result in a combination of dominant and recessive phenotypes.
Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Article
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- Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in aGenome research · 2024Article
- Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in abioRxiv : the preprint server for biology · 2024Article
- The Effect of theInternational journal of molecular sciences · 2023Article
- A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
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Abstract
Although mutations in the microtubules-associated protein Tau have long been connected with several neurodegenerative diseases, the underlying molecular mechanisms causing these tauopathies are still not fully understood. Studies in various models suggested that dominant gain-of-function effects underlie the pathogenicity of these mutants; however, there is also evidence that the loss of normal physiological functions of Tau plays a role in tauopathies. Previous studies on Tau in Drosophila involved expressing the human Tau protein in the background of the endogenous Tau gene in addition to inducing high expression levels. To study Tau pathology in more physiological conditions, we recently created Drosophila knock-in models that express either wildtype human Tau (hTau
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