ArticleCells2021
TDP-43 Regulation of AChE Expression Can Mediate ALS-Like Phenotype in Zebrafish.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Validation in Drosophila of the in silico predicted clomipramine as repurposable for SOD1-ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.Acta neuropathologica communications · 2025Article
- Molecular Mechanisms of Protein Aggregation in ALS-FTD: Focus on TDP-43 and Cellular Protective Responses.Cells · 2025Review
- Exploring the neuroprotective potential of KC14 peptide from Cyprinus carpio against oxidative stress-induced neurodegeneration by regulating antioxidant mechanism.Molecular biology reports · 2024Article
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- A comprehensive review of electrophysiological techniques in amyotrophic lateral sclerosis research.Frontiers in cellular neuroscience · 2024Review
- Diving deep: zebrafish models in motor neuron degeneration research.Frontiers in neuroscience · 2024Review
- Skeletal muscle in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2023Review
- Zebrafish as a Model Organism for Studying Pathologic Mechanisms of Neurodegenerative Diseases and other Neural Disorders.Cellular and molecular neurobiology · 2023Review
- TDP-43 dysregulation and neuromuscular junction disruption in amyotrophic lateral sclerosis.Translational neurodegeneration · 2022Review
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Modeling neuromuscular diseases in zebrafish.Frontiers in molecular neuroscience · 2022Review
- Development of a high-throughput tailored imaging method in zebrafish to understand and treat neuromuscular diseases.Frontiers in molecular neuroscience · 2022Article
- Liquid-Liquid Phase Separation of TDP-43 and FUS in Physiology and Pathology of Neurodegenerative Diseases.Frontiers in molecular biosciences · 2022Review
- Acetylcholinesterase Inhibitors in the Treatment of Neurodegenerative Diseases and the Role of Acetylcholinesterase in their Pathogenesis.International journal of molecular sciences · 2021Review
- Where and Why Modeling Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021Review
- Advances of Zebrafish in Neurodegenerative Disease: From Models to Drug Discovery.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
The "distal axonopathy" hypothesis in amyotrophic lateral sclerosis (ALS) proposes that pathological changes occur at the neuromuscular junction (NMJ) early in the disease. While acetylcholinesterase (AChE) plays an important role in the functionality of the NMJ, its potential role in ALS remains unexplored. Here, we identified AChE as a limiting factor regulating muscle/motor neuron connection in a vertebrate model of ALS. Knockdown of the TAR DNA-binding protein 43 (TDP-43) orthologue in zebrafish resulted in early defects of motor functions coupled with NMJ disassembly. We found that a partially depleted tdp-43 caused a decrease of ache expression. Importantly, human AChE overexpression reduced the phenotypic defects in the tdp-43 loss of function model, with amelioration of post- and pre-synaptic deficits at the NMJ. In conclusion, our results provide a better understanding of the role of TDP-43 in the NMJ organization and indicate AChE as a contributing factor in the pathology of ALS. In particular, it may be implicated in the early defects that characterize NMJs in this major neurodegenerative disorder.
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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.