An immunohistochemical study on nuclear bodies in neurodegenerativediseases with abnormal protein aggregates
| Project/Area Number |
23659184
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Human pathology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TOYOSHIMA Yasuko 新潟大学, 脳研究所, 准教授 (20334675)
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| Co-Investigator(Renkei-kenkyūsha) |
ONODERA Osamu 新潟大学, 脳研究所, 教授 (20303167)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脳 / 神経 / 神経変性疾患 / 多系統萎縮症 / 筋萎縮性側索硬化症 / 細胞内凝集体 / 核内小体 / 新経変性疾患 |
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| Research Abstract |
The kinetics of two nuclear bodies, PML and Cajal bodies, werestudied in multiple system atrophy (MSA) and sporadic amyotrophic lateral sclerosis (ALS),respectively. In MSA, in the nuclei of the pontine nuclei neurons, PML bodies were found tobe deformed in the presence of r-synuclein-positive intranuclear inclusions: the roundstructures changed to rod-like or linear abnormal ones. Statistically, the entire volume ofPML bodies was significantly decreased in MSA group (n=5) than in control group (n=5). InALS, in the nuclei of the lumbar anterior horn cells, the number of Cajal bodies was significantly decreased in ALS group (n=5: 8.06+/-4.41) than in control group (n=5:17.19+/-4.09). It is tempting to speculate that in MSA and ALS, these decreases of PML andCajal bodies, which are associated with neuronal viability, play an important role inneuronal cell death in relation to abnormalities of r-synuclein and TDP-43, respectively.
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Report
(3 results)
Research Products
(30 results)
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[Journal Article] Ubiquilin immunoreactivity in cytoplasmic and nuclear inclusions in synucleinopathies, polyglutamine diseases and intranuclear inclusion body disease.2012
Author(s)
Mori F, Tanji K, Odagiri S, Toyoshima Y, Yoshida M, Ikeda T, Sasaki H, Kakita A, Takahashi H, Wakabayashi K.
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Journal Title
Acta Neuropathol
Volume: 124
Issue: 1
Pages: 149-151
DOI
Related Report
Peer Reviewed
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[Journal Article] The potential of GPNMB as novel neuroprotective factor in amyotrophic lateral sclerosis.2012
Author(s)
Tanaka H.. Shimazawa M., Kimura M., Takata M., Tsuruma K, Yamada M., Takahashi H., Hozumi I., Niwa J., Iguchi Y., Nikawa T., Sobue G., Inuzuka T. and Hara H.
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Journal Title
Scientific Reports
Volume: 2
Issue: 1
Pages: 573-573
DOI
Related Report
Peer Reviewed
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[Journal Article] Primary lateral sclerosis : Upper-motor-predominant amyotrophic lateral sclerosis with frontotemporal lobar degeneration-immunohistochemical and biochemical analyses of TDP-432011
Author(s)
Kosaka T, Fu YJ, Shiga A, Ishidaira H, Tan CF, Tani T, Koike R, Onodera O, Nishizawa M, Kakita A, Takahashi H
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Journal Title
Neuropathology. 2011
Volume: 32
Issue: 4
Pages: 373-384
DOI
Related Report
Peer Reviewed
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