biostudies-literatureUnknown64Ma J<h4>Background</h4>Apolipoprotein E deficiency (ApoE^-/-) increases progressively iron in the liver, spleen and aortic tissues with age in mice. However, it is unknown whether ApoE affects brain iron.<h4>Methods</h4>We investigated iron contents, expression of transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), iron regulatory proteins (IRPs), aconitase, hepcidin, Aβ42, MAP2, reactive oxygen species (ROS), cytokines and glutathione peroxidase 4 (Gpx4) in the brain of ApoE^-/- mice.<h4>Results</h4>We demonstrated that ApoE^-/- induced a significant increase in iron, TfR1 and IRPs and a reduction in Fpn1, aconitase and hepcidin in the hippocampus and basal ganglia. We also showed that replenishment of ApoE absent partly reversed the iron-related phenotype in ApRedox biology102779https://www.ebi.ac.uk/biostudies/studies/S-EPMC10363452biostudies-literatureApolipoprotein E is required for brain iron homeostasis in mice.PMC10363452Li WQian ZMZhong QXShen MQMa JGuo QfalseApolipoprotein E is required for brain iron homeostasis in mice.<h4>Background</h4>Apolipoprotein E deficiency (ApoE^-/-) increases progressively iron in the liver, spleen and aortic tissues with age in mice. However, it is unknown whether ApoE affects brain iron.<h4>Methods</h4>We investigated iron contents, expression of transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), iron regulatory proteins (IRPs), aconitase, hepcidin, Aβ42, MAP2, reactive oxygen species (ROS), cytokines and glutathione peroxidase 4 (Gpx4) in the brain of ApoE^-/- mice.<h4>Results</h4>We demonstrated that ApoE^-/- induced a significant increase in iron, TfR1 and IRPs and a reduction in Fpn1, aconitase and hepcidin in the hippocampus and basal ganglia. We also showed that replenishment of ApoE absent partly reversed the iron-related phenotype in Ap2023-01-01T00:00:00Z2023 Aug2025-04-05T12:35:41.604Z2025-04-05T12:35:41.604ZS-EPMC103634523733955810.1016/j.redox.2023.102779