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Despite years of study, ApoE still has secrets to give up. At the 14th International Conference on Alzheimer’s and Parkinson’s Diseases, held March 27–31 in Lisbon, Portugal, researchers indicted ApoE4 on several fronts. They charged it with holding back the microglial response to amyloidosis. They said it bungled disposal of damaged mitochondria, perhaps perturbing cellular energy metabolism. They implicated it in axonal remodeling, and said this may explain why the highly arborized neurons of the entorhinal cortex are particularly vulnerable to Alzheimer’s. Finally, as peripheral ApoE is beginning to attract more attention, scientists are accounting for the different pools of this lipoprotein that course through the human body. Others elaborated on how ApoE4 damages blood vessels in the brain and correlates with neuroinflammation. Quite the rap sheet.