2006 Fiscal Year Final Research Report Summary
Analyses of nodal sodium currents and establishment of effective treatment for diabetic neuropathy
| Project/Area Number |
17590862
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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 |
KUWABARA Satoshi Chiba University, Department of Neurology・Graduate School of Medicine, Associate Professor, 大学院医学研究院, 助教授 (70282481)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Masahiro Chiba University, Department of Neurology, Graduate School of Medicine, Assistant Professor, 大学院医学研究院, 助手 (70345023)
KANAI Kazuaki Chiba University, Chiba University Hospital, Senior Neurologist, 医学部附属病院, 医員 (10375751)
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| Project Period (FY) |
2005 – 2006
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| Keywords | diabetes / neuroscience / Neurophysiology / neuromuscular disease |
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| Research Abstract |
(1)Using a computerized current measurement system, we established in vivo measurements of axonal ionic currents. We performed this measurements in 100 normal control subjects, and determined the normal value of this assessment.
(2)Patients with diabetic neuropathy (N=100) showed significantly smaller axonal sodium currents, fast potassium currents, and slow potassium currents than normal controls subjects. The extent of the reduced sodium currents significantly correlate with the state of glycemic controls. These results have been published in international journals (Misawa S, Kuwabara S, et al., Clinical Neurophysiology 2005,2006).
(3)Metabolic abnormalities in diabetic nerves are mediated by an enzyme, aldose reductase. Inhibitor of this enzyme (aldose reductase inhibitor : ARI) is now clinically available. We found that nerve conduction velocities and axonal nodal sodium currents improve after administration of ARI. We have published the data in an international journal (Misawa S, Kuwabara S, et al., Neurology 2006).
(4)In patients with severe axonal degeneration, intervention for enhancement of axonal regeneration is required. For the first step, we have assessed the effects of Rho-kinase inhibitor that promotes axonal regeneration in the central nervous system, in experimental neuropathy. We found that this agent significantly enhances peripheral nerve regeneration in a mouse Wallerian degeneration model, and published in an international journal (Hiraga A, Kuwabara S, et al., Journal of Peripheral Nervous System, 2006)
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