University of California, Berkeley scientists have for the first time used CRISPR-Cas9 gene editing to disable a defective gene that causes amyotrophic lateral sclerosis, or Lou Gehrig’s disease, in mice, extending their lifespan by 25 percent. The therapy delayed the onset of the muscle wasting that characterizes the disease, which results in progressive weakness and eventually proves fatal when the muscles that control breathing fail. This step toward a CRISPR cure for human ALS will be reported Dec. 20 in the journal Science Advances. The mice were genetically engineered to express a mutated human gene that in humans causes about 20 percent of all inherited forms of the disease and about 2 percent of all cases of ALS worldwide. Though the genetic cause is not known for all cases of ALS, all are accompanied by the premature death of motor neurons in the brain stem and spinal cord. The neurons allow the brain to control muscles, so loss of this connection means loss of...