Loss of ATP13A2 function leads to lysosomal polyamine sequestration, depleting cytosolic polyamines in astrocytes. This triggers compensatory polyamine biosynthesis, diverting SAM from DNA methylation and promoting neuroinflammation.
The protocol studies the impact of different levels of recombinant human CXCL1 on midbrain neurons from iPSCs using conditioned media from ATP13A2WT astrocytes.
