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Increased Rac1 activity may also exacerbate AD symptoms through free radicals in astrocytes as Rac1 was required for A-induced production of reactive oxygen species in these cells (Lee et al., 2002)

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Bloodbrain barrier disruption in PD has been modeled with a human BBB-on-chip cultivated under flow conditions and containing iPSC-derived dopaminergic neurons, astrocytes, microglia, and pericytes differentiated with cell-specific chemically defined medium and hBECs using Qian's method from patients