Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival

被引:82
|
作者
Weydt, P
Hong, SY
Witting, A
Möller, T
Stella, N
Kliot, M
机构
[1] Univ Washington, Dept Neurol, Seattle, WA 98195 USA
[2] Univ Washington, Dept Neurol Surg, Seattle, WA 98195 USA
[3] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA
[4] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA
来源
AMYOTROPHIC LATERAL SCLEROSIS | 2005年 / 6卷 / 03期
关键词
motor neuron disease; cannabinoids; therapy; mouse model;
D O I
10.1080/14660820510030149
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Therapeutic options for amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disorder, remain limited. Emerging evidence from clinical studies and transgenic mouse models of ALS suggests that cannabinoids, the bioactive ingredients of marijuana ( Cannabis sativa) might have some therapeutic benefit in this disease. However, Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the predominant cannabinoid in marijuana, induces mind-altering effects and is partially addictive, compromising its clinical usefulness. We therefore tested whether cannabinol (CBN), a nonpsychotropic cannabinoid, influences disease progression and survival in the SOD1 (G93A) mouse model of ALS. CBN was delivered via subcutaneously implanted osmotic mini-pumps ( 5 mg/kg/day) over a period of up to 12 weeks. We found that this treatment significantly delays disease onset by more than two weeks while survival was not affected. Further research is necessary to determine whether non-psychotropic cannabinoids might be useful in ameliorating symptoms in ALS.
引用
收藏
页码:182 / 184
页数:3
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