Scarred blood vessels may be one clue to APOE4’s Alzheimer’s risk
Scientists know APOE4 raises Alzheimer’s risk. A surprising change in blood vessel cells may help explain how.
A new study published in Alzheimer's & Dementia has uncovered insights into how the APOE4 gene, a well-known genetic risk factor for Alzheimer's disease, impacts brain immune cells called microglia. The research, conducted by scientists at the University of Colorado Anschutz and Pacific Northwest National Laboratory, reveals that ApoE4 alters the way brain cells handle fat, leading to inflammation and potentially contributing to the onset of Alzheimer's.
Microglia, the brain's cleanup and security crew, are crucial in maintaining brain health. When exposed to ApoE4, these cells store fat differently, forming fewer but larger fat droplets and experiencing a reduced number of mitochondria, which are responsible for energy production. This change in fat handling depends on whether ApoE4 is carrying fat or is fat-free.
When carrying fat, ApoE4 changes how cells store and use fat and energy. In contrast, when it's fat-free, it triggers a stronger immune response, resulting in inflammation.
Kimberley D. Bruce, a senior author of the study and an associate professor in endocrinology at CU Anschutz School of Medicine, explains that these findings suggest that how ApoE4 handles fat may influence the brain's immune cells' behavior. The study highlights that inflammation and changes in how brain cells use and store fat could be linked to Alzheimer's disease.
While the research doesn't prove that APOE4 causes Alzheimer's, it offers a potential explanation for how this genetic risk factor affects brain function and inflammation.
Bruce suggests that in the future, researchers could explore ways to help ApoE4 carry more fat to maintain microglia function and explore treatments to reduce inflammation triggered by fat-free ApoE4, ultimately aiming to lower Alzheimer's risk in individuals carrying the APOE4 gene. However, the study emphasizes that more research is needed to confirm these findings in human subjects and to determine their implications for Alzheimer's disease prevention or treatment.
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