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

Patrick Weydt; Soyon Hong; Anke Witting; Thomas Möller; Nephi Stella; Michel Kliot

doi:10.1080/14660820510030149

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

Patrick Weydt^*, Soyon Hong, Anke Witting, Thomas Möller, Nephi Stella, Michel Kliot

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

94 Scopus citations

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.

Original language	English (US)
Pages (from-to)	182-184
Number of pages	3
Journal	Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders
Volume	6
Issue number	3
DOIs	https://doi.org/10.1080/14660820510030149
State	Published - Sep 2005
Externally published	Yes

Funding

This work was supported by a Leopoldina Fellowship (to PW), Mary Gates Scholarship (to SH), University of Washington Royalty Research Fund (to TM), Project ALS (to MK) and Valerie Estess (to PW and MK). We thank Drs. A. La Spada and G. Carter for comprehensive discussion.

Keywords

Cannabinoids
Motor neuron disease
Mouse model
Therapy

ASJC Scopus subject areas

Clinical Neurology

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10.1080/14660820510030149

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title = "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.",

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AU - Stella, Nephi

AU - Kliot, Michel

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N2 - 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.

AB - 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.

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

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