2002 Fiscal Year Final Research Report Summary
A study of galectin-1 as a possible therapeutic agent for amyotrophic lateral sclerosis
| Project/Area Number |
13670629
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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 | Yamagata University |
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Principal Investigator |
KATO Takeo Yamagata University, Faculty of Medicine, Professor, 医学部, 教授 (90194828)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Kaoru Yamagata University, Faculty of Medicine, Professor, 医学部, 教授 (30234975)
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| Project Period (FY) |
2001 – 2002
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| Keywords | amyotrophic lateral sclerosis / galectin-1 / motor neuron disease / oxidized galectin-1 / reduced galectin-1 |
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| Research Abstract |
Background and purpose
Abnormal accumulation of neurofilaments in motor neurons is a characteristic pathological finding in amyotrophic lateral sclerosis (ALS). Recently we revealed that oxidized galectin-1, which has axonal regeneration-enhancing activity, accumulates in the neurofilamentous lesions in ALS. The objective of this study was to investigate whether oxidized galectin-1 has a beneficial effect on ALS.
Methods
Oxidized recombinant human galectin-1 (rhGAL-1/ox) or physiological saline was injected into the left gastrocnemius muscle of transgenic mice with a mutant SOD1 (H46R), an animal model of ALS.
Results
Administration of rhGAL-1/ox to the mice delayed the onset of motor dysfunction and prolonged the life of the mice and the duration of their illness. Motor neurons of the lumbar cord were more preserved in the mice injected with rhGAL-1/ox than in those injected with physiological saline.
Conclusion
The study suggests that rhGal-1/ox administration could be a new therapeutic strategy for ALS.
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