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Furthermore, dysfunctional cholesterol metabolism, mediated by ApoE, particularly the ApoE4 variant, disrupts lipid homeostasis, leading to excessive LDs accumulation in microglia and astrocytes (Qi et al., 2021)
J Immunol 182, 44794487, doi: 10.4049/jimmunol.0713927 (2009)
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Many studies have shown a link between the risk of cardiovascular diseases and the production of TMA by intestinal bacteria, which is further converted to trimethylamine N-oxide (TMAO) by hepatic enzymes (Tang et al
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