| Project/Area Number |
23659458
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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 |
Neurology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KAJI Ryuji 徳島大学, ヘルスバイオサイエンス研究部, 教授 (00214304)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Satoshi 徳島大学, 大学院ヘルスバイオサイエンス研究部, 特任教授 (50240916)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWARAI Toshitaka 徳島大学, 大学院ヘルスバイオサイエンス研究部, 講師 (50614137)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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 | ＴＮＦα / ＡＬＳ / ＳＯＤ１ / adalizumab / ALS / therapy / SOD1 tansgenic mouse |
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| Research Abstract |
Mouse anti-TNF alpha antibody was intraperitoneally administered to SOD1 mice, which are widely used for animal model for amyotrophic lateral sclerosis. We physiologically and pathologically evaluated the efficacy of the therapy or suppression of disease progression. No significant result was obtained in physiological evaluations, including life span, body weight and motor functions. However, pathological examination revealed partial ameliorative response, including the numbers of survival motor neurons and the reactive gliosis. These results further supported involvement of neuroinflammation in motor neuron death by mutant SOD1 probably at the end stage. Evaluation of the downstream cascades, such as NF kappa, JNK-AP-1 and caspase 3, is necessary to optimize the therapy using the anti-TNF alpha antibody.
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