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

Pizzasegola, C., Caron, I., Daleno, C., Ronchi, A., Minoia, C., Carri', M.t., et al. (2009). Treatment with lithium carbonate does not improve disease progression in two different strains of SOD1 mutant mice. AMYOTROPHIC LATERAL SCLEROSIS, 10(4), 221-228 [10.1080/17482960902803440].

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

CARRI', MARIA TERESA;
2009-08-01

Abstract

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 of autophagy and the promotion of mitochondriogenesis and neurogenesis. This prompted us to test the lithium effect also in female SOD1G93A mice with two phenotypes of different disease severity. Female SOD1G93A mice of C57BL/6J or 129S2/Sv genetic background were treated daily with Li(2)CO(3) 37 mg/kg (1 mEq/kg) i.p. starting from age 75 days until death. Grip strength, latency to fall on rotarod and body weight were monitored twice weekly. At the time of death the spinal cord was removed to assess the number of motor neurons and to measure the expression of a marker of autophagy (LCII) and the activity of mitochondrial complex IV. We observed a significant anticipation of the onset and reduced survival in 129Sv/G93A and no effect in C57/G93A mice treated with lithium compared to vehicle treated mice. Moreover, lithium neither exerted neuroprotective effects nor increased the expression of LCII and the activity of mitochondrial complex IV in the spinal cord. The present study does not identify any therapeutic or neuroprotective effect of lithium in SOD1G93A female mice.
ago-2009
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10 - BIOCHIMICA
English
Con Impact Factor ISI
Superoxide Dismutase; Animals; Spinal Cord; Humans; Disease Progression; Disease Models, Animal; Lithium Carbonate; Mice; Mice, Transgenic; Antimanic Agents; Behavior, Animal; Phenotype; Body Weight; Survival Rate; Amyotrophic Lateral Sclerosis; Mice, Inbred C57BL; Biological Markers; Female; Male
Pizzasegola, C., Caron, I., Daleno, C., Ronchi, A., Minoia, C., Carri', M.t., et al. (2009). Treatment with lithium carbonate does not improve disease progression in two different strains of SOD1 mutant mice. AMYOTROPHIC LATERAL SCLEROSIS, 10(4), 221-228 [10.1080/17482960902803440].
Pizzasegola, C; Caron, I; Daleno, C; Ronchi, A; Minoia, C; Carri', Mt; Bendotti, C
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/68193
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