| Project/Area Number |
15300118
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Tokyo Metropolitan Organization for Medical Research |
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Principal Investigator |
UCHIHARA Toshiki Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience, Neuropathology, Staff Scientist, 東京都神経科学総合研究所, 副参事研究員 (10223570)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Ayako Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience, Neuropathology, Chief Technician, 研究員 (90301796)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 2005: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | CAG repeat disease / nuclear inclusion / multifluorolabeling / three dimensional reconstruction / silver staining / tauopathy / シヌクレイノパチー / SCA1 / Catalyzed reporter deposition |
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| Research Abstract |
1.Triple-immunofluorolabeling was achieved through amplification of one or two of the signals with catalyzed reporter deposition method (J Histochem Cytochem 2003:51:1201-6, J Neurosci Methods 2004:135:67-70). This allowed supersensitive detection of the signals distinguishable from non amplified signals even if the two signals were probed with antibodies from the same species.
2.On pontine neurons of SCA1 brains, transactional area of nuclei containing nuclear inclusions (NIs) was quantified and was compared with that of neurons not containing NIs. Larger transactional area was correlated with the presence of NI, suggesting that NI is related to neuroprotection rather than neuronal death. (J Neurol Neurosurg Psychiatry 2003:74:597-601, Adv Neurol Res 2004:48:334-345)
3.An old autopsy case of Heredoataxie cerebelleuse de Pierre Marie was reevaluated and found to be indistinguishable from Machado-Joseph disease (Arch Neurol 2004:61:784-790)
4.Tau deposition in cerebral infarction or inflammatory process was found to be distinguishable from degenerative tauopathy in terms of the absence of phosphorylation and fibrillary structure.
5.Deposit of 4-repeat tau was found to be correlated with argyrophilia with Gallyas silver method (Acta Neuropathol 2005:109:299-305, ibid 2005:110:158-164, J Neurol Sci in press) and that of 3-repeat tau with Campbell method (Acta Neuropathol 2005:109:483-489, Handbook of Clinical Neurol in press)
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