that, like rodent cells, they also showed decreased viability with 25% of human dopaminergic cells dying due to A1-induced toxicity (Fig. 4e). This death could not be attributed to Il-1α, TNFα, and C1q alone, which did not cause death of cells in purified cultures. Death was blocked by caspase-2/-3 inhibitors but not by necrostatin or glutamate blockers and thus appeared to be due to apoptosis (Extended Data Fig. 9). Thus, A1s secrete a soluble toxin that rapidly kills a subset of CNS neurons and mature oligodendrocytes, but not other CNS cell types.
