ArticleBiological psychiatry2018
DOPA Decarboxylase Modulates Tau Toxicity.
Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 21 citations in OpenAlex.
- Dominant α-tubulin mutations rescue tauopathy neurodegenerative phenotypes inbioRxiv : the preprint server for biology · 2026Article
- Endoplasmic reticulum unfolded protein response transcriptional targets of XBP-1s mediate rescue from tauopathy.Communications biology · 2024Article
- L-DOPA regulates neuroinflammation and Aβ pathology through NEP and ADAM17 in a mouse model of AD.Molecular brain · 2024Article
- Transgenic Dendra2::tau expression allows in vivo monitoring of tau proteostasis in Caenorhabditis elegans.Disease models & mechanisms · 2024Article
- Expression of Human L-Dopa Decarboxylase (DDC) under Conditions of Oxidative Stress.Current issues in molecular biology · 2023Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Loss of aly/ALYREF suppresses toxicity in both tau and TDP-43 models of neurodegeneration.GeroScience · 2022Article
- Distinct Poly(A) nucleases have differential impact on sut-2 dependent tauopathy phenotypes.Neurobiology of disease · 2021Article
- Compound screening in cell-based models of tau inclusion formation: Comparison of primary neuron and HEK293 cell assays.The Journal of biological chemistry · 2020Article
- Synergistic toxicity between tau and amyloid drives neuronal dysfunction and neurodegeneration in transgenic C. elegans.Human molecular genetics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe microtubule-associated protein tau accumulates into toxic aggregates in multiple neurodegenerative diseases. We found previously that loss of D
methodsTo better understand how loss of D
resultsWe identified one dopamine synthesis gene, DOPA decarboxylase (DDC), as a suppressor of tau toxicity in tau transgenic worms. Loss of the C. elegans DDC gene, bas-1, ameliorated the behavioral deficits of tau transgenic worms, reduced phosphorylated and detergent-insoluble tau accumulation, and reduced tau-mediated neuron loss. Loss of function in other genes in the dopamine and serotonin synthesis pathways did not alter tau-induced toxicity; however, their function is required for the suppression of tau toxicity by bas-1. Additional loss of D
conclusionsLoss of the DDC bas-1 reduced tau-induced toxicity in a C. elegans model of tauopathy, while loss of no other dopamine or serotonin synthesis genes tested had this effect. Because loss of activity upstream of DDC could reduce suppression of tau by DDC, this suggests the possibility that loss of DDC suppresses tau via the combined accumulation of dopamine precursor levodopa and serotonin precursor 5-hydroxytryptophan.
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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.