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. 2019 Feb 11;11:14. doi: 10.3389/fnagi.2019.00014

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Copyright © 2019 Fernandez, Hamby, McReynolds and Ray.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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APOE4 disrupts homeostatic pathways in astrocytes and microglia to cause neurodegeneration and AD. APOE4 expression and the normal aging process itself impair astrocyte and microglia physiology in specific pathways, which could theoretically be targeted to treat AD. In addition to deficient clearance of Aβ, emerging evidence specifically highlights lipid dysregulation and deficient glucose metabolism in astrocytes, and a neurodegenerative pro-inflammatory response in microglia, and to some extent in astrocytes as well. All of these pathways converge with similar deficits that occur in normal aging to ultimately lead to neurodegeneration.