Project/Area Number |
21591342
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | 独立行政法人国立病院機構(静岡てんかん・神経医療センター) (2011) National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders (2009-2010) |
Principal Investigator |
TAKAHASHI Yukitoshi 独立行政法人国立病院機構(静岡てんかん・神経医療センター), 臨床研究部, 部員(統括診療部長) (70262764)
|
Co-Investigator(Kenkyū-buntansha) |
NISHIMURA Shigeko 独立行政法人国立病院機構静岡てんかん・神経医療センター(臨床研究部), 臨床研究部, 室員 (60393120)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 急性脳炎 / 辺縁系脳炎 / 卵巣奇形腫 / GluRψ2(NR2B) / GluRζ1(NR1) / アポトーシス / サイトカイン / GluRε2(NR2B) / GluRε2 (NR2B) / GluRζ1 (NR1) |
Research Abstract |
In CSF from patients with non-herpetic acute limbic encephalitis(NHALE), antibodies to GluRψ2(NR2B) and GluRζ1(NR1) we re related with clinical evolution. Antibodies to NMDAR seemed to internalize extra-synaptic NMDAR, because those antibod i es prevent ed apoptosis of rat cultured neurons. Those antibodies seemed not to inte rnalize synaptic NMDAR, because those did not affect phosphorylation of CREB(cAMP-Responsive-Element-Binding protein). These may contribute to the relatively better outcome of NHALE.
|