| Project/Area Number |
15591151
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Shizuoka Institute of Epilepsy and Neurological Disorders |
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Principal Investigator |
TAKAHASHI Yukitoshi Shizuoka Institute of Epilepsy and Neurological Disorders, National Epilepsy Center, Senior Director of Research, てんかん神経医療センター臨床研究部), 部長 (70262764)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Tateki Shizuoka Institute of Epilepsy and Neurological Disorders, National Epilepsy Center, Researcher, てんかん神経医療センター臨床研究部)・遺伝子生化学研究室, 室長 (40045513)
TANAKA Masaki Shizuoka Institute of Epilepsy and Neurological Disorders, National Epilepsy Center, Director of Research, てんかん神経医療センター臨床研究部)・薬理研究室, 室長 (90360809)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Acute encephalitis / Acute encephalopathy / Lombic encephalitis / Glutamate receptor / Autoimmunity / Epilepsy / Mental retardation / Motor disturbance / 自己抗体 |
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| Research Abstract |
1. Methods and Patients
We have studied autoantibodies against GluRε2 and GluRδ2 in sera and cerebrospinal fluids (CSFs) (500 samples) from 121 patients with acute encephalitis and 6 patients with acute encephalopathy. Those samples were donated from many doctors in all over Japan. Using tetracycline-induction system, we established stable NIH3T3 transformant cell lines expressing NMDA-type GluRε2 subunit or GluRδ2. Cell extracts of the transformants were transferred to the nitrocellulose membrane to detect the presence of antibodies against GluRs. The membrane was reacted with serum or CSF from patients, and was stained by second antibodies coupled to alkaline phosphatase.
2. Results
We divided 43 patients with acute encephalitis or encephalopathy, whose CSFs were examined, into localized encephalitis and whole spread encephalitis, clinically. The former manifested psychic symptoms or illusion or solitary convulsion without apparent impairment of consciousness in the initial stage of encephalitis. The latter manifested profound loss of consciousness from the onset of encephalitis. In patients with localized encephalitis, autoantibodies against GluRε2 in sera and CSFs were not related with their prognoses. The autoantibodies against GluRε2 became positive in acute and recovery stages. In patients with whole spread encephalitis, autoantibodies against GluRε2 in sera were not related with their prognoses, but those in CSFs were significantly related with prognoses. The autoantibodies against GluRε2 became positive in recovery and chronic stages. Autoantibodies against GluRε2 in CSFs were related with significantly with mental retardation and epilepsy onset in chronic stages, but insignificantly with motor disturbance in chronic stages.
3. Hypotheses
Autoantibodies against GluRε2 in CSFs might contribute to the onset of encephalitis in localized encephalitis including limbic encephalitis, and to the sequelae in whole spread encephalitis.
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