Mutations of Cu,Zn superoxide dismutase cause an autosomal dominant form of familial amyotrophic lateral sclerosis. An animal model of the disease has been produced by expressing mutant human SOD1 in transgenic mice (G93A). In order to quantify the dysfunction of the motor unit in transgenic mice, e
Effect of rosmarinic acid in motor dysfunction and life span in a mouse model of familial amyotrophic lateral sclerosis
β Scribed by Yosuke Shimojo; Kunio Kosaka; Yoshihiro Noda; Takahiko Shimizu; Takuji Shirasawa
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 385 KB
- Volume
- 88
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
Amyotrophic lateral sclerosis (ALS) is a lateβonset progressive neurodegenerative disease affecting motor neurons. About 2% of patients with the disease are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1). The purpose of this study is to assess the effect of rosemary extract and its major constituents, rosmarinic acid (RA) and carnosic acid (CA), in human SOD1 G93A transgenic mice, which are wellβestablished mouse models for ALS. The present study demonstrates that intraperitoneal administration of rosemary extract or RA from the presymptomatic stage significantly delayed motor dysfunction in paw grip endurance tests, attenuated the degeneration of motor neurons, and extended the life span of ALS model mice. In addition, RA administration significantly improved the clinical score and suppressed body weight loss compared with a vehicleβtreated group. In conclusion, this study provides the first report that rosemary extract and, especially, RA have preventive effects in the mouse model of ALS. Β© 2009 WileyβLiss, Inc.
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