Rina Takano

TL;DR: Astrocytic damage reflected by elevated CSF glial fibrillary acidic protein is a clinically relevant, primary pathologic process in neuromyelitis optica, and is far more severe than demyelination.

TL;DR: IHN could be a clinical marker for the early phase of an exacerbation of neuromyelitis optica and the early initiation of the treatment could prevent subsequent neurological damage.

TL;DR: CSF-GFAP and S100B may be clinically useful biomarkers in NMO, and astrocytic damage is strongly suggested in the acute phase of NMO.

TL;DR: It is proposed that NMO should be classified as an astrocytopathic disease rather than a demyelinating disease because recent experimental studies have convincingly shown that AQP4 antibody is pathogenic in causing astorocytic destruction and dysfunction in vitro, ex vivo and in vivo.

TL;DR: This study revealed that the G3370T mutation was associated with milder forms of MM and the G3510A mutation wasassociated with a more severe form.