2005 Fiscal Year Final Research Report Summary
A study for detection of an auto-antigen which is causative agents in acute inflammatory demyelinating polyneuropathy
| Project/Area Number |
16590813
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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 |
Neurology
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| Research Institution | Chiba University |
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Principal Investigator |
HATTORI Takamichi Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (30114317)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Masahiro Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (70345023)
KUWABARA Satoshi Chiba University, Graduate School of Medicine, Assistant Professor, 大学院・医学研究院, 助教授 (70282481)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Guillain-Barre syndrome / SEREX |
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| Research Abstract |
Guillain-Barre syndrome currently divided into demyelinating and axonal forms; acute inflammatory demyelinating polyneuropathy (AIDP) and acute axonal motor neuropathy (AMAN). Target molecules in cases of AMAN has been recognized to be ganliosides, expresses on the motor axolemma. In contrast, target molecules in cases of AIDP have not been identified. We investigated about the new auto-antigen, which is a key molecule for pathogenesis of Guillain-Barre syndrome.
We have investigated about the difference between the demyelinating and axonal subtypes of Guillain-Barre syndrome for a long time (Kuwabara S, et al. Ann Neurol 2002;52:180-7, Ogawara K, et al. Ann Neurol 2000;48:624-31). As part of preparation for the investigation about the new antigen, we collected clinical, laboratory, and electrophysiological data on 131 GBS patients. From these data, we have investigated and reported about the difference of patterns and speeds of progression in the demyelinating and the axonal subtypes of Guillain-Barre syndrome (Hiraga A, et al. Neurology 2005;64:856-860), and elucidated the patterns and sequential changes in electrodiagnostic abnormalities of Guillain-Barre syndrome (Hiraga A, et al J Neurol Neurosurg Psychiatry 2005;76:719-22). Moreover, we have reviewed the epidemiology, immunopathogenesis, clinical spectrum and treatment of Guillain-Barre syndrome (Kuwabara S. Drugs 2004;64:597-610).
Next, we obtained serum samples from 37 healthy control, and 40 patients with demyelinating form of Guillain-Barre syndrome (AIDP), and stored them at-80℃. cDNA library was synthesized from glioma cell line. And, we applied serological analysis of recombinant cDNA expression libraries (SEREX) to AIDP. We identified independent 7 cDNA clones that potentially encoded pathogenetic antigens in AIDP. We are going to perform an enzyme-linked immunosorbent assay for serum antibodies to the proteins from cDNA clones.
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