Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease arising from a progressive loss of motor neurons in the motor cortex, brainstem and spinal cord, leading to atrophy of limb, axial and respiratory muscles. The cause of motor neuron degeneration remains largely unknown and to date there is no potent therapy. Some familial cases of ALS are caused by dominant mutations in the gene encoding superoxide dismutase (SOD1). Overexpression of SOD1 gene mutations in mice and rats recapitulates the clinical and pathological characteristics of ALS and therefore constitute useful models of ALS to screen therapeutical approaches.
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