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New antisense oligonucleotide therapies reach first base in ALS

Two studies highlight the evolution of antisense oligonucleotide therapy for amyotrophic lateral sclerosis, offering hope for an effective treatment.

In 1993, mutations in the superoxide dismutase 1 (SOD1) gene were the first genetic cause identified in amyotrophic lateral sclerosis (ALS), a neurological disease characterized by rapidly progressive paralysis and death from respiratory failure1,2.

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