CORD-19:16a812de72963ceda960a168236e8dbe91832d45 / 0-630 JSONTXT

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{"project":"Epistemic_Statements","denotations":[{"id":"T1","span":{"begin":328,"end":484},"obj":"Epistemic_statement"}],"text":"Remyelination as Neuroprotection\n\nAbstract\n\n\nA major area of investigation in the neurosciences is directed at understanding the factors that participate in neurological deficits. In demyelinating diseases of the central nervous system (CNS), it has been assumed that demyelination by itself contributes to functional deficits. Previous physiological studies demonstrated that demyelination in the CNS can result in conduction slowing and conduction block (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). Howeve"}

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{"project":"CORD-19-PD-HP","denotations":[{"id":"T1","span":{"begin":183,"end":196},"obj":"Phenotype"},{"id":"T2","span":{"begin":268,"end":281},"obj":"Phenotype"},{"id":"T3","span":{"begin":377,"end":390},"obj":"Phenotype"},{"id":"T4","span":{"begin":562,"end":575},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/HP_0011096"}],"text":"Remyelination as Neuroprotection\n\nAbstract\n\n\nA major area of investigation in the neurosciences is directed at understanding the factors that participate in neurological deficits. In demyelinating diseases of the central nervous system (CNS), it has been assumed that demyelination by itself contributes to functional deficits. Previous physiological studies demonstrated that demyelination in the CNS can result in conduction slowing and conduction block (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). Howeve"}

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