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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.1
- 수록면
- 181 - 186 (6page)
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초록· 키워드
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Background and Purpose: N-methyl-D-aspartate (NMDA)-mediated neurotoxicity and oxidative stress have
been implicated in the etiology of amyotrophic lateral sclerosis (ALS). Memantine is a low-affinity, noncompetitive
NMDA receptor antagonist that may protect against motor neuron degeneration.
Methods: Thirty transgenic mice expressing the G93A SOD1 mutation were randomly divided into control, lowdose
memantine (30 mg/kg/day), and high-dose memantine (90 mg/kg/day) groups, with memantine supplied daily
with drinking water beginning at 75 days of age. Body weight, survival, and behavioral performances including a
rotarod test, paw grip endurance, and hindlimb extension reflex were assessed in the control and memantine-diet
groups.
Results: Clinical symptoms were evident in the G93A transgenic mice by 11 weeks of age. Memantine was
tolerated well. Compared to control, mice treated with memantine performed better in the rotarod test and hindlimb
extension reflex. Moreover, low-dose memantine treatment significantly prolonged the survival of the transgenic mice
relative to control mice (141 vs 134 days, p<0.05).
Conclusion: These findings suggest that memantine, even when administered at the time of symptom onset, has
beneficial effects on patients with ALS.
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