Abstract
We investigated the effects of clenbuterol, a β2-adrenoceptor agonist with known anabolic and neuroprotective properties, on G93A-SOD1 mice, a transgenic murine model of familial amyotrophic lateral sclerosis (ALS). Relative to saline-treated vehicle controls (0.2 ml/kg/day; i.p.), early pathologic G93A-SOD1 mice treated with clenbuterol (1.5 mg/kg/day; i.p.) demonstrated a delayed onset of hindlimb signs as measured by rotarod performance, slowed disease progression, as well as trends toward mitigated losses of lumbar motoneurons and body weight. Responses in female G93A-SOD1 mice were favorable to those of males, suggesting synergistic effects between clenbuterol and sex-specific factors. Overall, our data suggest that clenbuterol offers therapeutic effects on ALS-related neuromuscular degeneration.
Original language | English |
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Pages (from-to) | 155-158 |
Number of pages | 4 |
Journal | Neuroscience Letters |
Volume | 397 |
Issue number | 1-2 |
DOIs | |
State | Published - 10 Apr 2006 |
Externally published | Yes |
Keywords
- Amyotrophic lateral sclerosis
- Clenbuterol
- Dimorphism
- G93A-SOD1 transgenic mice
- Spinal cord