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

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
pathways. These results highlight the potential beneficial role of Aβ in
cellular function, as well as its complex effects on cellular and
organismal physiology that must be considered when using C. elegans as a
model for Alzheimer’s Disease.