GFAP and neuromyelitis optica: Subsequently, a passive-transfer mouse model of NMO involving intracranial injection of NMO-IgG and human complement recapitulated key pathological findings in NMO, including loss of AQP4 and glial fibrillary acidic protein (GFAP) immunoreactivity, granulocyte and macrophage infiltration, vasculocentric deposition of activated complement, and demyelination [23].