ArticlePloS one2019
Caenorhabditis elegans hub genes that respond to amyloid beta are homologs of genes involved in human Alzheimer's disease.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- The amino acid substitutions A30W, K28A, and M35C alter amyloid-β peptide toxicity in cell culture and in anFrontiers in aging neuroscience · 2026Article
- Exploring the therapeutic potential ofFrontiers in pharmacology · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Multi-Modal Locomotion of Caenorhabditis elegans by Magnetic Reconfiguration of 3D Microtopography.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Article
- Exploring the conservation of Alzheimer-related pathways between H. sapiens and C. elegans: a network alignment approach.Scientific reports · 2021Article
- Activation of Microbiota Sensing - Free Fatty Acid Receptor 2 Signaling Ameliorates Amyloid-β Induced Neurotoxicity by Modulating Proteolysis-Senescence Axis.Frontiers in aging neuroscience · 2021Article
- Unearthing of Key Genes Driving the Pathogenesis of Alzheimer's Disease via Bioinformatics.Frontiers in genetics · 2021Article
- Positive association between soil arsenic concentration and mortality from alzheimer's disease in mainland China.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020Article
- Identification of Hub Genes Related to Alzheimer's Disease and Major Depressive Disorder.American journal of Alzheimer's disease and other dementiasArticle
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prominent characteristic of Alzheimer's disease (AD) is the accumulation of amyloid beta (Abeta) proteins in the form of plaques that cause molecular and cellular alterations in the brain. Due to the paucity of brain samples of early-stage Abeta aggregation, animal models have been developed to study early events in AD. Caenorhabditis elegans is a genetically tractable animal model for AD. Here, we used transcriptomic data, network-based protein-protein interactions and weighted gene co-expression network analysis (WGCNA), to detect modules and their gene ontology in response to Abeta aggregation in C. elegans. Additionally, hub genes and their orthologues in human and mouse were identified to study their relation to AD. We also found several transcription factors (TFs) responding to Abeta accumulation. Our results show that Abeta expression in C. elegans relates to general processes such as molting cycle, locomotion, and larval development plus AD-associated processes, including protein phosphorylation, and G-protein coupled receptor-regulated pathways. We reveal that many hub genes and TFs including ttbk-2, daf-16, and unc-49 have human and mouse orthologues that are directly or potentially associated with AD and neural development. In conclusion, using systems biology we identified important genes and biological processes in C. elegans that respond to Abeta aggregation, which could be used as potential diagnostic or therapeutic targets. In addition, because of evolutionary relationship to AD in human, we suggest that C. elegans is a useful model for studying early molecular events in AD.
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