Although the mechanism for the metabolism of fatty acids in hyperactive neurons has been recently elucidated (according to this mechanism, fatty acids coupled with ApoE-positive lipid droplets are discarded from neurons, endocytosed by neighboring astrocytes, and metabolized through oxidative phosphorylation, ultimately leading to activation of molecular pathways to overcome fatty acid toxicity, and, in turn, protect neuronal function [215]), its relevance for AD neurodegeneration requires further investigation. Here, APOE is linked to Alzheimer disease.