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Further studies have shown that early hyperactivation of insulin signaling may cause negative feedback mediated by mTOR and decreased biliverdin-A reductase (BVR-A) activity, an oxidative stress-sensitive antioxidant enzyme and second messenger in insulin signaling, controlling IRS1 and Akt serine phosphorylation [207,208]

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As the brain’s consumption and metabolism of ARA are up-regulated in AD patients, suggesting that ARA is involved in the pathomechanism of this disease (Esposito et al., 2008), ARA consumption could constitute a risk factor for AD in humans and should be considered in future preventive strategies