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Im thinking about the study using a typhoid vaccine as a model of acute inflammation that showed people with GCH1 variants werent able to increase BH4 levels enough to prevent endothelial dysfunction.[ref] Add to this the reduction in Bifidobacterium seen in severe SARS-CoV-2 infection[ref] The Immune System and Tetrahydrobiopterin: I mentioned above in the Nitric Oxide section that BH4 can be oxidized to BH2 during inflammation and that AGMO plays a role in modulating platelet-activating factor in immune system activation

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More recent findings suggest that ferroptosis, the iron accumulation-related and lipid peroxidation-driven type cell death pathway [9, 10], plays an important role in AD pathology [11]