Treatment with lithium carbonate does not improve disease progression in two different strains of SOD1 mutant mice.

摘要: It has been shown that chronic treatment with lithium carbonate (Li(2)CO(3)) in presymptomatic SOD1G93A transgenic male mice, a model of ALS, was able to remarkably increase their lifespan through the activation autophagy and promotion mitochondriogenesis neurogenesis. This prompted us test effect also female mice two phenotypes different disease severity. Female C57BL/6J or 129S2/Sv genetic background were treated daily Li(2)CO(3) 37 mg/kg (1 mEq/kg) i.p. starting from age 75 days until death. Grip strength, latency fall on rotarod body weight monitored twice weekly. At time death spinal cord removed assess number motor neurons measure expression marker (LCII) activity mitochondrial complex IV. We observed significant anticipation onset reduced survival 129Sv/G93A no C57/G93A compared vehicle mice. Moreover, neither exerted neuroprotective effects nor increased LCII IV cord. The present study does not identify any therapeutic