Vitamin E depletion is associated with subclinical axonal degeneration in juvenile horses.
Vitamin E depletion is associated with subclinical axonal degeneration in juvenile horses.
复制标题
维生素 E 消耗与幼年马的亚临床轴突变性有关。
DOI：
10.1111/evj.13907
复制
发表时间：
2023
影响因子：
2.2
通讯作者：
Finno,CarrieJ
中科院分区：
文献类型：
--
作者：
Donnelly,CallumG;Finno,CarrieJ
研究背景磷酸化神经丝重蛋白是神经轴索损伤的标志物，在马神经轴索营养不良的马中增加。然而，在这方面，目的测量马神经轴索营养不良易感性的纳塔尔后窗口期幼年马驹的血清和脑脊液磷酸化神经丝重浓度。研究设计病例-对照体内实验研究。方法使用从13匹马驹收集的冷冻血清和脑脊液测量磷酸化神经丝重的浓度在维生素E缺乏的环境中从1到6个月大。其中4匹马驹由受马神经轴索营养不良影响的母鼠生产，出现了与马神经轴索营养不良一致的临床体征，并经组织病理学确诊。剩下的9匹由健康的母马生产的马驹，维生素E耗尽，临床上保持健康。一个额外的队列的马驹，由健康的马，补充维生素E（α-生育酚; α-TOH）从出生和采样similarly.ResultsSerum α-TOH浓度显着较高的维生素E补充健康马驹。在任何时间点，血清磷酸化神经丝重浓度在组间均无显著差异。健康维生素E耗竭马驹脑脊液磷酸化神经丝重浓度随年龄增加（p< 0.001）;主要限制补充维生素E的遗传易感队列无法用于比较。结论我们证明，维生素E缺乏可能会提高脑脊液磷酸化神经丝重在其他健康的少年马驹在6个月大的时候。我们强调了一个重要的辅因子时，考虑解释脑脊液磷酸化神经丝重浓度在少年马。
BackgroundPhosphorylated neurofilament heavy, a marker of neuroaxonal damage, is increased in horses with equine neuroaxonal dystrophy. However, the temporal dynamics of this biomarker during the post‐natal risk period are not understood.ObjectiveTo measure serum and cerebrospinal fluid phosphorylated neurofilament heavy concentrations in juvenile foals across the post‐natal window of susceptibility for equine neuroaxonal dystrophy.Study designCase–control in vivo experimental study.MethodsConcentrations of phosphorylated neurofilament heavy were measured using frozen serum and cerebrospinal fluid collected from 13 foals raised in a vitamin E deficient environment from 1 to 6 months of age. Four of these foals were produced by equine neuroaxonal dystrophy‐affected dams, developed clinical signs consistent with equine neuroaxonal dystrophy and had a diagnosis confirmed by histopathology. The remaining nine foals, produced by healthy mares, were vitamin E depleted and remained clinically healthy. An additional cohort of foals, produced by healthy mares, were supplemented with vitamin E (α‐tocopherol; α‐TOH) from birth and sampled similarly.ResultsSerum α‐TOH concentrations were significantly higher in vitamin E supplemented healthy foals. Serum phosphorylated neurofilament heavy concentrations did not differ significantly between groups at any time point. Cerebrospinal fluid phosphorylated neurofilament heavy concentrations increased with age in healthy vitamin E depleted foals (p< 0.001); an effect that was not observed in healthy vitamin E supplemented foals.Main limitationsA genetically susceptible cohort supplemented with vitamin E was not available for comparison.ConclusionWe demonstrate that vitamin E depletion may elevate cerebrospinal fluid phosphorylated neurofilament heavy in otherwise healthy juvenile foals by 6 months of age. We highlight an important cofactor to consider when interpreting cerebrospinal fluid phosphorylated neurofilament heavy concentrations in juvenile horses.