Vitamin E depletion is associated with subclinical axonal degeneration in juvenile horses.
Authors: Donnelly Callum G, Finno Carrie J
Journal: Equine veterinary journal
Summary
Equine neuroaxonal dystrophy (eNAD) represents a significant welfare concern in juvenile foals, yet the biochemical cascade leading to axonal damage remains incompletely characterised. Donnelly and Finno investigated whether vitamin E deficiency triggers subclinical neuroaxonal degeneration by measuring phosphorylated neurofilament heavy (pNfH)—a sensitive marker of axonal injury—in serum and cerebrospinal fluid (CSF) across the critical 1–6 month post-natal window. Using foals deliberately raised in vitamin E-depleted conditions, they compared three cohorts: four genetically susceptible foals that developed clinical eNAD, nine vitamin E-depleted but clinically healthy foals, and a vitamin E-supplemented control group. Whilst serum pNfH showed no between-group differences, CSF pNfH concentrations rose significantly with age in vitamin E-deficient healthy foals (p<0.001), an effect absent in supplemented controls—suggesting subclinical axonal pathology develops before overt clinical signs manifest. These findings emphasise that CSF pNfH interpretation in juvenile horses must account for vitamin E status as a confounding factor, and indicate that adequate α-tocopherol availability during early development may be critical for preventing neuroaxonal degeneration independent of genetic predisposition.
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Practical Takeaways
- •Vitamin E supplementation from birth should be considered a critical management factor for foals, as deficiency may trigger subclinical neuroaxonal damage detectable in cerebrospinal fluid even before clinical signs appear
- •When interpreting cerebrospinal fluid phosphorylated neurofilament heavy concentrations in juvenile horses with suspected neuroaxonal dystrophy, vitamin E status must be evaluated as a potential confounding factor
- •This biomarker's elevation in CSF may represent subclinical axonal damage rather than clinical disease in vitamin E deficient foals, warranting nutritional intervention as a preventive strategy
Key Findings
- •Cerebrospinal fluid phosphorylated neurofilament heavy concentrations increased significantly with age in vitamin E depleted healthy foals (p<0.001) but not in supplemented foals
- •Serum phosphorylated neurofilament heavy did not differ significantly between vitamin E depleted and supplemented groups at any time point
- •Four foals with equine neuroaxonal dystrophy from affected dams developed clinical signs confirmed by histopathology, while nine vitamin E depleted foals from healthy mares remained clinically healthy
- •Vitamin E depletion may elevate cerebrospinal fluid phosphorylated neurofilament heavy in otherwise healthy juvenile foals by 6 months of age