Study offers new clues about how genetic risk for Alzheimer's affects brain immune cells
Researchers have identified how the APOE4 gene variant disrupts lipid processing in the brain's immune cells, known as microglia. This dysfunction leads to inflammation and may explain the increased risk of Alzheimer's disease associated with this genetic factor.
Why it matters
Understanding the mechanism behind APOE4 could lead to new therapeutic targets for preventing or treating Alzheimer's disease.
by Laura Kelley, University of Colorado Anschutz
edited by Gaby Clark , reviewed by Andrew Zinin
This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:
Add to Preferred Sources Lipid-free ApoE4 leads to increased lipid-droplet accumulation, whereas reconstituted high-density lipoprotein (HDL)-like particles (rHDL) lead to enhanced lipid (POPC) uptake by primary microglia. Credit: Alzheimer's & Dementia (2026). DOI: 10.1002/alz.71882 Researchers at the University of Colorado Anschutz and Pacific Northwest National Laboratory have found a new clue that may help explain why some people are more likely to develop Alzheimer's disease. It suggests that a protein linked to the disease can change how the brain's immune cells handle fat and trigger inflammation. Those changes could help explain how a well-known genetic risk factor for Alzheimer's affects the brain.
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