Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 67, Issue 3, Pages 1021-1034Publisher
IOS PRESS
DOI: 10.3233/JAD-180820
Keywords
Alzheimer's disease; ApoE; inflammation; lipid droplets; microglia
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Funding
- University of Kansas Alzheimer's Disease Center [P30AG035982]
- First Affiliated Hospital of Zhengzhou University
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [T32HD057850] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P30AG035982] Funding Source: NIH RePORTER
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Recent association studies indicate several genes highly expressed by microglia influence Alzheimer' s disease (AD) risk, which suggests microglial function contributes to this disease. Here, we evaluated how one component of microglial function, cytokine release, affects AD-related phenomena. First, we used a 3-hour lipopolysaccharide (LPS) treatment to activate mouse BV2 microglial cells. Next, we removed the LPS-containing medium, added LPS-free medium, and after 6 hours collected the medium conditioned by the activated BV2 microglial cells. We then exposed human neuronal SH-SY5Y cells to the conditioned medium for 24 hours. At the end of the 24-hour exposure, we assessed amyloid-beta protein precursor (A beta PP), tau, apolipoprotein E (ApoE), and lipid status. The amount of A beta PP was unaffected, although a slight decrease in soluble A beta PPia suggested a subtle reduction in A beta PP non-amyloidogenic processing occurred. Tau mRNA increased, but total and phosphorylated tau levels were unchanged. ApoE mRNA increased, while ApoE protein levels were lower. Per cell lipid droplet number decreased and lipid oxidation increased. These results show cytokine release by activated microglial cells can influence specific AD-relevant physiologies and pathologies.
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