Article
Mutant SOD1 knockdown in all cell types ameliorates disease in G85R SOD1 mice with a limited additional effect over knockdown restricted to motor neurons.
Journal of neurochemistry - 1 Apr 2010
Wang Lijun, Grisotti Gabriella, Roos Raymond P
Abstract excerpt
Approximately 10% of patients with amyotrophic lateral sclerosis (ALS) have familial ALS (FALS), and 20% of FALS is caused by mutant Cu/Zn superoxide dismutase type 1 (MTSOD1). Previous studies have convincingly demonstrated that MTSOD1 expression in other cell types besides motor neurons (MNs) contributes to disease in MTSOD1 FALS transgenic mice. Using Cre/LoxP methods, we knocked down G85R SOD1 mRNA by 66% in...
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