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In amyotrophic lateral sclerosis (ALS) caused by SOD1 gene mutations, both cell‐autonomous and noncell‐autonomous mechanisms lead to the selective degeneration of motoneurons (MN). Here, we evaluate the therapeutic potential of gene therapy targeting mutated SOD1 in mature astrocytes using mice expressing the mutated SOD1G93A protein. An AAV‐gfaABC1D vector encoding an artificial microRNA is used...