Reduced cerebral blood flow and metabolic rate trigger an adaptive mitochondrial remodeling program in a Down syndrome mouse model

In the Dp16(1)Yey/+ Down syndrome mouse model, reduced cerebral blood flow and oxygen metabolic rate occur, with effects more pronounced in males than females.

• Why it matters: Mitochondrial dysfunction is central to Down syndrome, but brain-wide links between trisomy 21, bioenergetics, and compensatory mitochondrial responses remain unclear.
• What they did: The study used MRI to measure cerebral blood flow and oxygen metabolic rate, then assessed mitochondrial respiratory capacity and ATP synthase activity across brain regions alongside transcriptomic profiling of mitochondrial OXPHOS and proteostasis pathways.
• The result: Despite suppressed oxygen metabolism, mitochondrial respiratory capacity and ATP synthase activity are largely preserved, while mitochondrial OXPHOS genes are upregulated, suggesting an adaptive remodeling program that does not fully normalize metabolic dysfunction.

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