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Targeting mitochondrial function holds great promise for the dual prevention of CVDs and cognitive decline

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Given that some mutant enzymes retain low-level FAD-binding capacity, a gene + high-dose riboflavin synergy strategy has been proposed: in AIFM1 encephalopathies, low-level AAV transduction re-establishes baseline protein expression, while daily riboflavin doses above 400 mg act as a molecular chaperone to stabilize FAD binding a regimen shown to improve ICARS scores and neuroimaging outcomes (54, 75)

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