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The Transcriptomic and Proteomic Molecular Signatures of Equine Multiple-System Neuropathy (Grass Sickness)
Kim M Summers1, Anna E Karagianni2, Paula Ledesma Fernandez3
1Mater Research Institute-University of Queensland, Woolloongabba, QLD 4102, Australia.
Cells
|August 13, 2026
Summary
Equine grass sickness (EGS) involves neurodegeneration, likely from a plant toxin. This study reveals distinct gene and protein changes in affected horses, indicating cellular stress and inflammation.
Area of Science:
- Veterinary Neurology
- Molecular Pathology
- Equine Medicine
Background:
- Equine grass sickness (EGS), or equine dysautonomia, is a fatal neuropathy in horses.
- It is suspected to be caused by a neurotoxic phospholipase A2 (nPLA2).
- Understanding the molecular mechanisms of EGS neurodegeneration is crucial.
Purpose of the Study:
- To investigate neuronal gene and protein expression in EGS.
- To elucidate the molecular mechanisms of neurotoxicity and neurodegeneration in EGS.
- To identify molecular signatures associated with EGS.
Main Methods:
- Histological examination of cranial cervical ganglia from EGS and control horses.
- Transcriptomic analysis of neuronal tissue.
- Comparison with existing proteomic datasets and network analysis (BioLayout, Ingenuity Pathway Analysis).
Main Results:
- EGS horses exhibited typical EGS pathology in cranial cervical ganglia.
- Distinct gene and protein expression profiles were observed in EGS horses compared to controls.
- The EGS molecular signature included reduced expression of neurological function genes (ion channels, synaptic function, mitochondrial proteins) and increased expression of stress, cell death, and inflammation markers.
Conclusions:
- The identified molecular signature suggests widespread neurodegeneration in EGS.
- This study enhances understanding of the molecular changes in this neurotoxic, neurodegenerative disease.
- Findings provide insights into the pathogenesis of equine grass sickness.
