PubMed:28571798 JSONTXT

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    Inflammaging

    {"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":56},"obj":"Sentence"},{"id":"T2","span":{"begin":57,"end":209},"obj":"Sentence"},{"id":"T3","span":{"begin":210,"end":615},"obj":"Sentence"},{"id":"T4","span":{"begin":616,"end":844},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":56},"obj":"Sentence"},{"id":"T2","span":{"begin":57,"end":209},"obj":"Sentence"},{"id":"T3","span":{"begin":210,"end":615},"obj":"Sentence"},{"id":"T4","span":{"begin":616,"end":844},"obj":"Sentence"}],"text":"Olfactory vector hypothesis for encephalitis lethargica.\nViruses have long been implicated in the pathogenesis of classical encephalitis lethargica, which was first described by Constantin von Economo in 1917. In this article, I propose the hypothesis that an airborne virus travels along the olfactory conduit to infect the olfactory bulb; this local infection or induced neuroinflammation, in turn, retrogradely targets certain neuronal populations with sleep-wake regulatory functions in the hypothalamus and midbrain, leading to the development of wakeful inactivity, a hallmark clinical feature of the disease. Furthermore, the olfactory vector hypothesis may also explain the pathomechanism of the debilitating complication of the disease, i.e., postencephalitic parkinsonism, in terms of a recently discovered nigro-olfactory projection."}

    RDoCTask1SampleData

    {"project":"RDoCTask1SampleData","denotations":[{"id":"T1","span":{"begin":0,"end":56},"obj":"Sleep-Wakefulness"}],"text":"Olfactory vector hypothesis for encephalitis lethargica.\nViruses have long been implicated in the pathogenesis of classical encephalitis lethargica, which was first described by Constantin von Economo in 1917. In this article, I propose the hypothesis that an airborne virus travels along the olfactory conduit to infect the olfactory bulb; this local infection or induced neuroinflammation, in turn, retrogradely targets certain neuronal populations with sleep-wake regulatory functions in the hypothalamus and midbrain, leading to the development of wakeful inactivity, a hallmark clinical feature of the disease. Furthermore, the olfactory vector hypothesis may also explain the pathomechanism of the debilitating complication of the disease, i.e., postencephalitic parkinsonism, in terms of a recently discovered nigro-olfactory projection."}