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Query: UMLS:C0042875 (vitamin E deficiency)
916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Equine motor neuron disease (EMND) is a neurodegenerative disorder of the somatic lower motor neurons that results in a syndrome of diffuse neuromuscular disease in the adult horse. The aetiology of this disorder is unknown, although prior studies have suggested that a deficiency in the lipid antioxidant vitamin E (alpha-tocopherol) contributes to the development of EMND. This paper describes a case-control study designed to investigate the association between plasma vitamin E levels and the risk of EMND for horses. Signalment, plasma vitamin E levels at the time of referral, and information relative to dietary and management practices were collected from 53 horses diagnosed with EMND and 69 controls. The mean plasma vitamin E concentration in EMND cases was significantly lower than that of control horses. After controlling for other risk factors of EMND, there was a statistically significant association between plasma vitamin E levels and EMND, with the likelihood of the disease increasing as the vitamin E concentration decreased. These findings support the reported role of vitamin E deficiency as one of the risk factors for EMND.
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PMID:Association between plasma vitamin E concentration and the risk of equine motor neuron disease. 941 50

A group of Walker Hounds and Beagles that were fed a diet of table scraps were examined because of slow, progressive loss of vision. Clinical and microscopic features of the disease were correlated to the dogs' micronutrient status. Sensory retinal degeneration, predominantly in the central tapetal fundus, was found in all dogs, and severity of changes varied with age of the dog. Plasma, serum, and tissue concentrations of vitamin E were low in affected dogs (10 to 40% of control values). Lipofuscin accumulation was found on microscopic examination in retinal pigment epithelium, smooth muscle cells of the intestinal tract, and neurons of the CNS. Findings were consistent with nutritional vitamin E deficiency and oxidative injury to photoreceptors of the retina. Changes in these dogs were similar to those described for central progressive retinal atrophy and equine lower motor neuron disease, suggesting these diseases may share a common pathogenesis to vitamin E deficiency.
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PMID:Retinal degeneration associated with vitamin E deficiency in hunting dogs. 973 Dec 58

Our previous studies implicated vitamin E deficiency as a risk factor for equine motor neuron disease, a possible model of human amyotrophic lateral sclerosis, and showed direct effects of this deficiency on brain vascular endothelium. To gain better understanding of the pathogenesis of equine motor neuron disease, we determined the effects of dietary antioxidant insufficiency and the resultant brain tissue oxidative stress on blood-brain barrier permeability. Rats (n = 40) were maintained on a diet deficient of vitamin E for 36 to 43 weeks; 40 controls were fed a normal diet. Permeability of the blood-brain barrier in the cerebral cortex was investigated using rhodamine B, and lipid peroxidation was measured as a marker for oxidative stress. Animals on the vitamin E-deficient diet showed less weight gain and had higher brain lipid peroxidation compared with the controls. Fluorometric studies demonstrated greater rhodamine B in the perivascular compartment and central nervous system parenchyma in rats on the deficient diet compared with controls. These results suggest that a deficiency in vitamin E increases brain tissue oxidative stress and impairs the integrity of the blood-brain barrier. These observations may have relevance to the pathogenesis of amyotrophic lateral sclerosis and other neurologic diseases.
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PMID:The role of dietary antioxidant insufficiency on the permeability of the blood-brain barrier. 1901 44