TY - JOUR T1 - Myelin injury without astrocytopathy in neuroinflammatory disorders with MOG antibodies JF - Journal of Neurology, Neurosurgery & Psychiatry JO - J Neurol Neurosurg Psychiatry SP - 1257 LP - 1259 DO - 10.1136/jnnp-2015-312676 VL - 87 IS - 11 AU - Kimihiko Kaneko AU - Douglas Kazutoshi Sato AU - Ichiro Nakashima AU - Shuhei Nishiyama AU - Satoru Tanaka AU - Romain Marignier AU - Jae-Won Hyun AU - Luana Michelli de Oliveira AU - Markus Reindl AU - Thomas Seifert-Held AU - Maria Sepulveda AU - Sasitorn Siritho AU - Patrick Joseph Waters AU - Kazuhiro Kurosawa AU - Tetsuya Akaishi AU - Hiroshi Kuroda AU - Tatsuro Misu AU - Naraporn Prayoonwiwat AU - Thomas Berger AU - Albert Saiz AU - Ho Jin Kim AU - Kyoichi Nomura AU - Dagoberto Callegaro AU - Kazuo Fujihara AU - Masashi Aoki Y1 - 2016/11/01 UR - http://jnnp.bmj.com/content/87/11/1257.abstract N2 - Acquired inflammatory central nervous system (CNS) disorders include multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), transverse myelitis and other less prevalent disorders.1 Differential diagnosis between these entities may be challenging in some cases due to overlapping clinical characteristics.Antibodies against aquaporin-4 (AQP4-Ab) suggest the diagnosis of NMOSD and promote severe immune-mediated astrocyte damage. However, some patients who are clinically diagnosed with NMOSD are AQP4-Ab-seronegative despite the use of highly sensitive cell-based assays (CBAs); therefore, other CNS molecules may be implicated as autoimmune targets in such cases.Recently, we reported the presence of conformational-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) in a portion of AQP4-Ab-seronegative NMOSD,2 ADEM and ON cases, but these antibodies are not usually found in typical MS, using highly specific CBAs.Thus, it is interesting to study how MOG-Ab+ cases pathologically and immunologically differ from AQP4-Ab+ cases and MS cases. In this multicentre international collaborative study, we evaluated MOG-Ab and AQP4-Ab antibodies in the CSF, and compared markers of myelin and astrocyte damage in the CSF as well as other routine CSF parameters between the three groups.We enrolled a total of 90 patients diagnosed with acquired inflammatory CNS disorders and serum positivity for MOG-Ab or AQP4-Ab antibodies, using CBAs from Japan, Brazil, Republic of Korea, Spain, France, Austria and Thailand. For the European countries, serum antibody testing was performed in each respective country. We also included CSF samples from 40 relapsing-remitting patients with MS who fulfilled the 2010 McDonald criteria3 and 16 samples from patients with non-inflammatory neurological disorders (spinal cord infarction, cerebral infarction, spinocerebellar degeneration=2, Parkinson's disease=2, progressive supranuclear palsy=2, amyotrophic lateral sclerosis=2, Alzheimer dementia=1, NPH=1, migraine=2, somatoform disorder=2) as controls. All samples were shipped in dry ice to Sendai, Japan, and stored at −80°C … ER -