T-2 toxin in SH-SY5Y cells remodels APP/Tau via a CLOCK-p53-senescence axis
In SH-SY5Y neuroblastoma cells, low-dose T-2 toxin for 24 hours changed Alzheimer-relevant APP and Tau proteins, with a p53-centred stress response, altered CLOCK rhythm parameters and a senescence-like phenotype; senolytic post-treatment reduced these markers. [1]
Automatic summary · not editorially reviewed
The key findings
SH-SY5Y human neuroblastoma cells were treated with low-dose T-2 toxin (6 nM) for 24 hours. [1]
Full-length APP decreased early, while Tau phosphorylation and total Tau rose later and stayed elevated. [1]
Post-treatment with dasatinib and quercetin reduced SA-β-gal burden, dampened p53 signalling and improved the APP/Tau profile. [1]
The source at a glance
- Study type / format
- In vitro cell-culture experiment (abstract)
- Population / context
- SH-SY5Y human neuroblastoma cells in culture
- Summary based on
- Study abstract
- Original publication
- September 1, 2026
SH-SY5Y cells exposed to 6 nM T-2 toxin
The abstract describes a cell-culture experiment: SH-SY5Y human neuroblastoma cells were treated with low-dose T-2 toxin (6 nM) for 24 hours. Researchers then profiled Alzheimer-relevant protein changes together with transcriptomic, circadian and senescence-related readouts. The stated aim was to clarify how environmental mycotoxins perturb Alzheimer-relevant protein homeostasis, which the authors call proteostasis. This is a laboratory cell model, not a study of people.
Supporting source [1]
APP fell early, Tau phosphorylation rose later
According to the abstract, T-2 toxin remodelled APP and Tau homeostasis: full-length APP decreased early, while Tau phosphorylation and total Tau increased later and stayed elevated, with dynamic cytokine release. RNA sequencing at 12 hours showed a p53-centred stress response and enrichment of circadian-related pathways. CLOCK rhythmicity was preserved but reparameterized, with a marked phase shift and an elevated mesor. Disrupting CLOCK attenuated p53 induction and Tau elevation; inhibiting p53 partly restored APP and reduced Tau changes while reshaping CLOCK abundance and localization, consistent with cross-regulation.
Supporting source [1]
Senescence-like phenotype and senolytic post-treatment
The abstract reports a time-dependent senescence-like phenotype that CLOCK and/or p53 inhibition attenuated. Post-treatment with the senolytic drugs dasatinib and quercetin reduced SA-β-gal burden, dampened p53 signalling and improved the APP/Tau profile. The authors link T-2 toxin exposure to Alzheimer-relevant proteostasis remodelling through a CLOCK-p53-senescence axis and suggest circadian and senescence-targeting strategies as complementary intervention points. These are proposals from a cell model; they do not establish human benefit.
Supporting source [1]
How to interpret this
This is an abstract only; the full text was not reviewed. All findings come from SH-SY5Y neuroblastoma cells in culture, not from humans or animals, so they cannot establish human lifespan or Alzheimer's disease benefits. The abstract does not report sample sizes, replication or effect sizes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Nie T, Li J, Tan S, Chen S, Yang D, Nepovimova E, Wu Q, Kuca K. · europepmc.org · September 1, 2026