PDP1 and Alzheimer disease: The fact that SNOC also decreased the Cit/αKG ratio somewhat in AD‐hiN (Figure 2A, right‐hand panel, p = 0.0205) may indicate that the high levels of NO present at baseline in AD‐hiN coupled with the addition of the NO donor may create such high levels of S‐nitrosylating species that another level of block upstream from Aco/IDH develops that limits citrate production, e.g., via inhibition of pyruvate dehydrogenase (PDH, Figure 2A), which contains a DLD subunit that is S‐nitrosylated to a significant degree (p = 0.026) in human AD brain over control (Figure 1A).