2000 Fiscal Year Final Research Report Summary
Pathogenesis of cortical dysplasia caused by neuroadapted strain of mumps virus
| Project/Area Number |
11670757
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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 | Shiga University of Medical Science |
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Principal Investigator |
TAKANO Tomoyuki Shiga University of Medical Science, Research Associates, 医学部, 助手 (80236249)
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| Project Period (FY) |
1999 – 2000
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| Keywords | Schizencephaly / Mumps virus / Kilham strain / Cerebral cleft / Ventricular cleft / Cortical dysplasia |
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| Research Abstract |
The pathogenesis of cortical dysplasia was analyzed by examining the brain lesions produced by the infection of the Kilham strain of mumps virus during the period of neuronal migration in hamsters.
Mumps virus antigen was detected in the neuroepithelial cells within the ventricular zone, the choroid plexus in the lateral ventricles, and vimentin-immunoreactive radial glial fibers. The main pathological findings were cerebral hemorrhage, neuronal necrosis, microsulci on the cerebral cortex, and cleft formation through the entire thickness of the cerebral mantle. The clefts seen in these experiments were lined by embryonal elements such as neuroepithelial cells and germinal cells. Based on these results and the original definition by Yakovlev and Wadsworth, the following two conclusions were suggested. First, the mumps virus localized to the neuroepithelial cells within the ventricular zone and the radial glial fibers may induce a destructive process and subsequent anomalous neuronal migration, resulting in cleft formation. Second, the formation of the ventricular cleft extending to the pial surface, which should be complete before the cortical infolding appears, is necessary in order to produce the characteristic cleft in schizencephaly which is associated with the pial-ependymal seam.
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