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- W3158628889 abstract "Abstract Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are found in lesions of multiple sclerosis (MS) and of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and may contribute to the neuronal loss that underlies permanent impairment. These pathological changes are due to the neuroinflammation that characterizes MS and the strong interplay between the ER and mitochondria. We investigated whether immunomodulatory drug glatiramer acetate (GA) can reduce these changes in the spinal cords of chronic EAE mice by using routine histology, immunostaining, and electron microscopy. EAE spinal cord tissue exhibited increased infiltration/inflammation (upregulation of proinflammatory cytokines), demyelination, mitochondrial dysfunction (increased fission, decreased fusion, and increased biogenesis), ER stress, downregulation of NAD+ dependent pathways, and increased neuronal death. GA reversed these pathological changes, suggesting that immunomodulating therapy can attenuate ER stress, mitochondrial dysfunction, apoptotic cell death, and demyelination in the CNS and increase NAD+ utilizing activities by suppressing neuroinflammation." @default.
- W3158628889 created "2021-05-10" @default.
- W3158628889 creator A5026814056 @default.
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- W3158628889 creator A5086754121 @default.
- W3158628889 date "2021-05-04" @default.
- W3158628889 modified "2023-09-26" @default.
- W3158628889 title "Immunomodulatory Therapy with Glatiramer Acetate Reduces Endoplasmic Reticulum Stress and Mitochondrial Dysfunction in Experimental Autoimmune Encephalomyelitis" @default.
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- W3158628889 doi "https://doi.org/10.1101/2021.05.04.442578" @default.