Elevated mitochondrial metabolism in Down syndrome iPSCs reduces commitment to neuroectoderm.

Increased mitochondrial metabolism in Down syndrome iPSCs (3S-iPSCs) is linked to reduced commitment to neuroectoderm, with higher mitochondrial membrane potential and MCU-linked calcium uptake.

• Why it matters: Reduced neurogenesis in Down syndrome is a key developmental problem, but how early mitochondrial and signaling changes affect neuroectoderm commitment is unclear.
• What they did: The study compared 3S-iPSCs to isogenic euploid controls, measuring mitochondrial membrane potential and calcium uptake via MCU, then assessing proliferation, G1 timing, ciliation, and neuroectoderm commitment.
• The result: Inhibiting MCU or slowing 3S-iPSC proliferation increased ciliation and improved neuroectoderm commitment, supporting a mitochondria-to-cilia signaling axis dysregulated in DS iPSCs.

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