Abstract
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease. Underlying genetic pathomechanisms include the C9orf72 repeat expansion, the most frequent genetic cause of ALS (C9ALS) in Western countries. Despite recent progress in unraveling C9ALS pathogenesis, reliable disease models and disease-modifying therapies still lack. Here, we aim to model C9ALS in vitro using 3D human spinal cord organoids (SCOs).
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