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Amyloid β induces hormetic-like effects through major stress pathways in a C. elegans model of Alzheimer’s disease

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DataONE2024-12-06 更新2025-04-26 收录
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Amyloid β (Aβ) is a peptide known for its characteristic aggregates in Alzheimer’s Disease and its ability to induce a wide range of detrimental effects in various model systems. However, Aβ has also been shown to induce some beneficial effects, such as antimicrobial properties against pathogens. In this work, we explore the influence of Aβ in stress resistance in a C. elegans model of Alzheimer’s Disease. We found that C. elegans that express human Aβ exhibit increased resistance to heat and anoxia, but not to oxidative stress. This beneficial effect of Aβ was driven from Aβ in neurons, where the level of induction of Aβ expression correlated with stress resistance levels. Transcriptomic analysis revealed that this selective stress resistance was mediated by the Heat Shock Protein (HSPs) family of genes. Furthermore, neuropeptide signaling was necessary for Aβ to induce stress resistance, suggesting neuroendocrine signaling plays a major role in activating organismal stress response pa..., , , # Data for Amyloid β Induces Hormetic-Like Effects Through Major Stress Pathways in a C. elegans Model of Alzheimer’s Disease Data includes results from experiments using a C. elegans strain that expresses human amyloid-beta fluorescently labeled at substoichiometric ratios. Contact Adriana San Miguel ([[asanmig@ncsu.edu](mailto:asanmig@ncsu.edu)]) with any questions. This manuscript has been accepted for publication (12/2024): Lichty, J.D.; Mane, H., Yarmey, V.R., San Miguel, A. Amyloid β Induces Hormetic-Like Effects Through Major Stress Pathways in a C. elegans Model of Alzheimer’s Disease. PLOS One (accepted). Data files include all data presented in the above-referenced manuscript. ## DataSet\_Lichty\_et\_al\_2024.xlsx - Tabs Figure 1B, Figure 1C, Figure 1D | variables | units | description | | :------------------- | :---------: | :-------------------------------------------------------------...
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2024-12-07
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