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It is shown that microglia generated from FRDA patient-derived iPSCs exhibit a cell-autonomous pro-inflammatory phenotype in the absence of exogenous inflammatory stimuli.
This work identifies transcriptional pathways linking variants in definitive ALS genes to widespread coordinated co-expression activity driven by gene-specific transcriptional programs, and establishes a generalizable framework that is readily applicable across heritable diseases for the identification of disease-relevant molecular pathways and target genes.
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