A study of residual lesions in horses that recovered from clinical signs of chronic equine dysautonomia.
- Journal Article
Summary
Equine dysautonomia (ED), a condition that leads to the deterioration and loss of neurons responsible for regulating involuntary bodily functions in horses, was examined to understand how some horses recover despite significant neuron loss. This research uncovered evidence of incomplete recovery in horses that survived ED, with the nervous system still showing signs of damage.
Overview of the Research
The research utilized a prospective, case control design and included thirteen horses (group ED) that recovered from clinical signs of ED and six healthy, age-matched control horses (group C). The recovered horses had been diagnosed with ED roughly 10.3±5.2 years prior. The methods used in this research involved post-mortem examination, with the goal to assess lesions, autonomic neuron counts, interstitial cells of Cajal (ICC), and signs of neurodegeneration.
Methods
- Post mortem examination: Routine examination of deceased animals to understand underlying issues.
- Neuron counts: Counting of neurons in peripheral and enteric ganglia to gauge the extent of neuron loss.
- Immunohistochemical assessment: Study of protein markers to trace neural networks and identify ICC and neurodegeneration within the intestine. Specifically, the protein gene product (PGP) 9.5, ICC (c-kit), and markers of neurodegeneration (beta-amyloid precursor protein and ubiquitin) were assessed.
Result Findings
The results showed several post-mortem findings in the ED group, including small intestinal dilation, muscular hypertrophy, and gastric mucosal hypertrophy and ulceration. Neuron density was significantly lower in the ED group compared to the control group, with the density decrease particularly dramatic in the ileum portion of the intestine.
Outcome and Conclusion
Despite neuronal loss, the ICC in the muscularis externa, which are involved in maintaining gut motility, remained intact. This possibly explains how horses are able to survive and maintain gastrointestinal function after experiencing ED. However, the researchers did caution that beta-amyloid precursor protein and ubiquitin results did not indicate active neurodegeneration. This study suggested that further investigation into treatments that support the function of ICC may be beneficial for horses recovering from ED.
Cite This Article
Publication
Researcher Affiliations
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
- Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
MeSH Terms
- Amyloid beta-Protein Precursor / analysis
- Animals
- Biomarkers
- Case-Control Studies
- Disease Progression
- Enteric Nervous System / pathology
- Horse Diseases / pathology
- Horses
- Interstitial Cells of Cajal
- Intestines / cytology
- Intestines / innervation
- Neurons / pathology
- Primary Dysautonomias / pathology
- Primary Dysautonomias / veterinary
- Prospective Studies
- Proteins / analysis
- Proto-Oncogene Proteins c-kit / analysis
- Ubiquitin / analysis
Conflict of Interest Statement
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Citations
This article has been cited 1 times.- Atkins CN, Hahn CN, McGorum BC. Comparison of Dysautonomia Across Species: Current Knowledge and Future Research Opportunities. J Vet Intern Med 2025 Jul-Aug;39(4):e70140.