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Peer-reviewedCC BYMicroPublication biology

Effects of Glucose and Vitamin D ₃ on Heat Stress Resistance in a Caenorhabditis elegans Model of Polyglutamine Aggregation Disease.

  • London Blackwell1
  • Joseph Sharp1
  • Gisselle Hernandez1
  • Mindy Farris2
  1. 1Biology, University of Central Arkansas.
  2. 2Biology, University of Central Arkansas, Conway, AR, United States.
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Abstract

Polyglutamine (polyQ) diseases are the most common form of inheritable neurodegeneration. Neuronal protein aggregates strongly correlate with polyQ symptoms; pathways that protect against protein aggregation may help mitigate the symptoms of poly-Q or delay disease onset. We used a C. elegans polyQ model, exposed to a heat stressor, to test potential protective mechanisms: glucose and vitamin D₃ (VD₃) supplementation. Glucose enrichment further shortened post-heat stress lifespan, while VD₃ in moderate doses trended toward restoring polyQ post-stress lifespan back to wild-type levels. These results show effects of early-life interventions that could indicate aspects of polyQ pathogenesis mechanisms and treatment options.

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Cite

BibTeXRIS
BibTeX
@article{blackwell2026effects,
  title = {{Effects of Glucose and Vitamin D ₃ on Heat Stress Resistance in a Caenorhabditis elegans Model of Polyglutamine Aggregation Disease.}},
  author = {London Blackwell and Joseph Sharp and Gisselle Hernandez and Mindy Farris},
  journal = {MicroPublication biology},
  year = {2026},
  month = oct,
  doi = {10.17912/micropub.biology.002376},
  url = {https://europepmc.org/article/MED/42928783},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Effects of Glucose and Vitamin D ₃ on Heat Stress Resistance in a Caenorhabditis elegans Model of Polyglutamine Aggregation Disease.
AU  - London Blackwell
AU  - Joseph Sharp
AU  - Gisselle Hernandez
AU  - Mindy Farris
PY  - 2026
DA  - 2026/10/10
JO  - MicroPublication biology
DO  - 10.17912/micropub.biology.002376
UR  - https://europepmc.org/article/MED/42928783
AB  - Polyglutamine (polyQ) diseases are the most common form of inheritable neurodegeneration. Neuronal protein aggregates strongly correlate with polyQ symptoms; pathways that protect against protein aggregation may help mitigate the symptoms of poly-Q or delay disease onset. We used a C. elegans polyQ model, exposed to a heat stressor, to test potential protective mechanisms: glucose and vitamin D₃ (VD₃) supplementation. Glucose enrichment further shortened post-heat stress lifespan, while VD₃ in moderate doses trended toward restoring polyQ post-stress lifespan back to wild-type levels. These results show effects of early-life interventions that could indicate aspects of polyQ pathogenesis mechanisms and treatment options.
SN  - 2578-9430
ER  -