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  • Title: Caspase-12 cleavage and increased oxidative stress during motoneuron degeneration in transgenic mouse model of ALS.
    Author: Wootz H, Hansson I, Korhonen L, Näpänkangas U, Lindholm D.
    Journal: Biochem Biophys Res Commun; 2004 Sep 10; 322(1):281-6. PubMed ID: 15313203.
    Abstract:
    Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motoneurons in the spinal cord and brain stem. We have characterized motoneuron death in transgenic mice carrying the mutant human copper/zinc superoxide dismutase, as a model for familial ALS. Previous studies have shown the involvement of mitochondria in nerve cell demise in these animals. We report here an early cleavage of caspase-12, residing in the endoplasmic reticulum (ER), in the spinal cord during the course of the disease. Apart from caspase-12, caspase-9, and caspase-3 were activated in the transgenic ALS mice. Staining with an antibody for nitrotyrosine, as a marker for oxidative stress, showed a large increase in the ALS mice. The results indicate that oxidative and ER induced stress causing caspase-12 activation are involved in neuronal death and disease progression in ALS. Caspase-12 and the ER pathway for cell death may constitute potential novel targets for the treatment of ALS.
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