Increased survival and neuroprotective effects of BN82451 in a transgenic mouse model of Huntington's disease

被引:47
|
作者
Klivenyi, P
Ferrante, RJ
Gardian, G
Browne, S
Chabrier, PE
Beal, MF [1 ]
机构
[1] Cornell Univ, Dept Neurol & Neurosci, New York Presbyterian Hosp, Weill Med Coll, 525 E 68th St, New York, NY 10021 USA
[2] Bedford VA Med Ctr, Ctr Geriatr Res Educ & Clin, Bedford, MA USA
[3] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA
[4] Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA
[5] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA
[6] Inst Henri Beaufour, Dept Biochem Pharmacol, F-91952 Les Ulis, France
关键词
experimental therapeutics; huntington; inflammation; neurodegeneration; oxidative damage; transgenic mice;
D O I
10.1046/j.1471-4159.2003.t01-1-01868.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
There is substantial evidence that excitotoxicity and oxidative damage may contribute to Huntington's disease (HD) pathogenesis. We examined whether the novel anti-oxidant compound BN82451 exerts neuroprotective effects in the R6/2 transgenic mouse model of HD. Oral administration of BN82451 significantly improved motor performance and improved survival by 15%. Oral administration of BN82451 significantly reduced gross brain atrophy, neuronal atrophy and the number of neuronal intranuclear inclusions at 90 days of age. These findings provide evidence that novel anti-oxidants such as BN82451 may be useful for treating HD.
引用
收藏
页码:267 / 272
页数:6
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