Evidence of Oxidative Injury of the Spinal Cord in 2 Horses With Equine Degenerative Myeloencephalopathy

Wong, David M.; Ghosh, Alip; Fales-Williams, Amanda J.; Haynes, Joseph S.; Kanthasamy, Arthi

doi:10.1177/0300985812439074

Cited by 13 publications

(17 citation statements)

References 18 publications

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“…It is known that d -α-tocopherol (RRR-α-tocopherol) is the most potent, bioavailable isoform of vitE, 23 and that oxidative stress is occurring in the brainstem and spinal cord of eNAD/EDM affected horses. 4 , 35 Current research is ongoing to determine the exact cause of this oxidative injury and how vitE prevents such damage.…”

Section: Vitamin Ementioning

confidence: 99%

“…Case reports have demonstrated that eNAD/EDM affects horses globally. Equine NAD/EDM has been diagnosed in horses residing in New York, 5 , 13 , 20 California, 16 Nebraska, 31 Iowa, 4 the United Kingdom, 26 Italy, 28 and Spain. 25 Researchers have also studied eNAD/EDM in Iowa, 4 Minnesota, 3 California, 1,7,24,32 Oregon, 6 , 11 and Florida.…”

Section: Prevalencementioning

confidence: 99%

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Equine degenerative myeloencephalopathy: prevalence, impact, and management

Burns¹,

Finno²

2018

VMRR

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Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy is an inherited neurodegenerative disorder affecting many horse breeds. Clinical signs include a symmetric ataxia and an abnormal stance at rest, similar to cervical vertebral compressive myelopathy, equine protozoal myeloencephalitis, and equine herpesvirus 1 myeloencephalopathy. This review will provide an update on the disease prevalence, management, impact, and ongoing research.

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Section: Vitamin Ementioning

confidence: 99%

Section: Prevalencementioning

confidence: 99%

Equine degenerative myeloencephalopathy: prevalence, impact, and management

Burns¹,

Finno²

2018

VMRR

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“…Calretinin rapidly buffers calcium in neurons in addition to affecting intracellular calcium signals pre- and postsynaptically. 3 It could be hypothesized that the oxidative injury associated with EDM 19 could lead to calcium release from the endoplasmic reticulum, leading to increased cytosolic and mitochondrial calcium concentrations and subsequent neuronal death, as previously suggested for many neurodegenerative diseases in humans. 8 However, in the rat, axonal fibers within the dorsal and dorsolateral funiculi and those originating from the nucleus thoracicus are often immunoreactive for calretinin.…”

Section: Discussionmentioning

confidence: 89%

“…Additionally, the evaluation of diseased positive control horses, as a means of determining the specificity of the IHC findings for EDM, was not performed in the previous 2 studies evaluating IHC markers in EDM. 17,19 …”

Section: Discussionmentioning

confidence: 99%

Evidence of the Primary Afferent Tracts Undergoing Neurodegeneration in Horses With Equine Degenerative Myeloencephalopathy Based on Calretinin Immunohistochemical Localization

et al. 2015

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Equine degenerative myeloencephalopathy (EDM) is characterized by a symmetric general proprioceptive ataxia in young horses, and is likely underdiagnosed for 2 reasons: first, clinical signs overlap those of cervical vertebral compressive myelopathy; second, histologic lesions—including axonal spheroids in specific tracts of the somatosensory and motor systems—may be subtle. The purpose of this study was (1) to utilize immunohistochemical (IHC) markers to trace axons in the spinocuneocerebellar, dorsal column–medial lemniscal, and dorsospinocerebellar tracts in healthy horses and (2) to determine the IHC staining characteristics of the neurons and degenerated axons along the somatosensory tracts in EDM-affected horses. Examination of brain, spinal cord, and nerves was performed on 2 age-matched control horses, 3 EDM-affected horses, and 2 age-matched disease-control horses via IHC for calbindin, vesicular glutamate transporter 2, parvalbumin, calretinin, glutamic acid decarboxylase, and glial fibrillary acidic protein. Primary afferent axons of the spinocuneocerebellar, dorsal column–medial lemniscal, and dorsospinocerebellar tracts were successfully traced with calretinin. Calretinin-positive cell bodies were identified in a subset of neurons in the dorsal root ganglia, suggesting that calretinin IHC could be used to trace axonal projections from these cell bodies. Calretinin-immunoreactive spheroids were present in EDM-affected horses within the nuclei cuneatus medialis, cuneatus lateralis, and thoracicus. Neurons within those nuclei were calretinin negative. Cell bodies of degenerated axons in EDM-affected horses are likely located in the dorsal root ganglia. These findings support the role of sensory axonal degeneration in the pathogenesis of EDM and provide a method to highlight tracts with axonal spheroids to aid in the diagnosis of this neurodegenerative disease.

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“…1 The reactive nitrogen species peroyxynitrite is an important nitrating agent in vivo, thus making 3-NT a biomarker for endogenous peroxynitrite activity. 2,16 Lectin-based histochemistry has been used to suggest that the source of the pigment saccharides present in melanosis coli in humans originated from macrophage phagocytosis of apoptotic epithelial cells while also demonstrating that the pigments of melanosis coli have characteristics typical of both lipofuscin and ceroid. 4 Ceroid accumulation has been documented in the small intestine of dogs with intestinal leiomyometaplasia as well as in nutritional panniculitis in cats, mink, foals, and pigs.…”

Section: Discussionmentioning

confidence: 99%

Evidence of Oxidative Injury in Pigs With Melanosis Coli

et al. 2014

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Melanosis coli is a dark discoloration of the colon due to accumulation of pigment-laden macrophages in the lamina propria. Three case submissions were received where rectal discoloration was reported at slaughter in pigs from separate production systems and melanosis coli was confirmed microscopically. Tissues from affected and unaffected cohort pigs were evaluated for evidence of oxidative damage using immunohistochemical staining for 3-nitrotyrosine, 4-hyroxynonenol, and malondialdehyde. Affected colons had significantly greater immunolabeling for all 3 target compounds than unaffected colons (P .001, all analyses). Hepatic vitamin E levels were low in both affected and unaffected pigs, and there was a trend toward lower values in affected pigs. Given the limited number of slaughter-collected samples available for this investigation, further study is warranted to elucidate the possible association between low vitamin E concentrations and oxidative damage in cases of melanosis coli in pigs.

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Evidence of Oxidative Injury of the Spinal Cord in 2 Horses With Equine Degenerative Myeloencephalopathy

Cited by 13 publications

References 18 publications

Equine degenerative myeloencephalopathy: prevalence, impact, and management

Equine degenerative myeloencephalopathy: prevalence, impact, and management

Evidence of the Primary Afferent Tracts Undergoing Neurodegeneration in Horses With Equine Degenerative Myeloencephalopathy Based on Calretinin Immunohistochemical Localization

Evidence of Oxidative Injury in Pigs With Melanosis Coli

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