The analysis of genetic abnormality of the target molecule in neuroimmunological disease
| Project/Area Number |
17590905
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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 | Kinki Univeristy |
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Principal Investigator |
MIYAMOTO Katsuichi Kinki Univeristy, School of Medicine, Assistant Professor, 医学部, 講師 (50388526)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUNOKI Susumu Kinki Univeristy, School of Medicine, Professor, 医学部, 教授 (90195438)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Brain, Nerve / Peripheral Nerve / Gene / Immunology / Auto antibody / 抹消神経 |
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| Research Abstract |
We investigated whether the anti-myelin antibody is present in multiple sclerosis (MS) or chronic inflammatory demyelinating polyneuropathy (CIDP) patients. We screened anti-myelin antibody in the sera of 90 MS patients and 10 CIDP patients by ELISA. We used peptides of myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), proteolipid protein (PLP) for MS patients, and PMP-22, PO glycoprotein (P0), P2 glycoprotein, Connexin-32 for CIDP patients. As for MS, 2 patients were seropositive for IgG antibody to MOG, 4 patients for IgG antibody to MBP, and 5 patients for IgG antibody to PLP. No relation between antibody titer and clinical severity was observed. In contrast, no CIDP patients had antibodies agains peripheral myelin peptides. Finally we could not provide evidence between the titer of the antibody and the character of MS.
Next, we analyzed the relationship with hereditary neuropathy and CIDP. We found two patients that they have heterozygous point mutation in the PO gene with similar clinical characters similar to CIDP. Especially an elderly woman with the heterozygous Thr124Met point mutation in the PO gene presented an axonal neuropathy with bilateral Adie's pupils, esophageal achalasia, hypotonic intestine, hypohidrosis and neurogenic bladder. She also showed demyelinating neuropathy with temporal dispersions and conduction blocks electrophysiolosically, which is typical of CIDP. In addition, reactivity of T cells against PO-peptides was elevated in this patient. This case indicated that the heterozygous PO gene mutation itself could induce auto-immunological reaction to develop CIDP through T cell activation against PO-protein.
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Report
(3 results)
Research Products
(3 results)
