Fig. 9
From: A novel Alzheimer’s disease drug candidate targeting inflammation and fatty acid metabolism
CAD-31 modifies lipid metabolism as a possible mechanism for neural protection. Free fatty acids are conjugated to carnitine for transport across the mitochondrial membrane. Once inside the mitochondria they can be metabolized to acetyl-coenzyme A (acetyl-CoA), which can then be transformed into ketone bodies. Acetyl-CoA can also be used by acetyl-coenzyme A carboxylase 1 (ACC-1) to form long-chain fatty acids. Adenosine monophosphate-activated protein kinase (AMPK) is able to phosphorylate ACC-1, inhibiting its function, which leads to an increase in available acetyl-CoA and ketone bodies. CAD-31 induces the activation of AMPK and modifies downstream genes. Acetyl-CoA and ketone bodies are able to be transported into the brain and have been shown to be neuroprotective