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

Abstract

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, Δ⁹‐tetrahydrocannabinol (Δ⁹‐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 non‐psychotropic 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.

• Motor neuron disease
• cannabinoids
• therapy
• mouse model