Amyotrophic lateral sclerosis (ALS) is actually a neurodegenerative ailment characterized Estrogen Receptor inhibitor mechanism by motor neuron death. ALS is usually induced by mutations inside the superoxide dismutase one gene (SOD1). Evidence for that non-cell-autonomous nature of ALS emerged from the observation that wild-type glial cells extended the survival of SOD1 mutant motor neurons in chimeric mice. To uncover Tyrosine hydroxylase the contribution of astrocytes to human motor neuron degeneration, we cocultured hESC-derived motor neurons with human major astrocytes expressing mutated SOD1. We detected a selective motor neuron toxicity that was correlated with elevated inflammatory response in SOD1-mutated astrocytes. Furthermore, we present evidence that astrocytes can activate NOX2 to produce superoxide and that result could be reversed by antioxidants. We present that NOX2 inhibitor, apocynin, can protect against the reduction of motor neurons brought about by SOD1-mutated astrocytes. These outcomes offer an assay for drug screening working with a human ALS in vitro astrocyte-based cell model.