Stephanie L. Baringer

AD Alzheimer's disease APP amyloid precursor protein Aβ amyloid-β BBB blood–brain barrier CM conditioned medium DMT1 divalent metal transporter ECs endothelial cells FTH ferritin heavy chain FTL ferritin light chain Fpn ferroportin Heph hephaestin iPSC induced pluripotent stem cell IL-1β interleukin-1β IL-6 interleukin-6 IRP iron response protein LDH lactate dehydrogenase NEP-1 neprilysin RRID Research Resource Identifier, see scicrunch.org sAPP-α soluble APP-α TfR transferrin receptor Tf...

References Kim Y, Connor JR. The roles of iron and HFE genotype in neurological diseases. Mol Aspects Med. 2020;75: 100867. Article CAS PubMed Google Scholar Wade QW, Chiou B, Connor JR. Iron uptake at the blood–brain barrier is influenced by sex and genotype. Adv Pharmacol. 2019;84:123–45. Article CAS PubMed Google Scholar Chiou B, Neal EH, Bowman AB, et al. Endothelial cells are critical regulators of iron transport in a model of the human blood–brain barrier. J Cereb Blood Flow Metab. 2019;39:2117–31.

Abstract Excessive brain iron accumulation is observed in early in the onset of Alzheimer's disease, notably prior to widespread proteinopathy. These findings suggest that increases in brain iron levels are due to a dysregulation of the iron transport mechanism at the blood-brain barrier. Astrocytes release signals (apo- and holo-transferrin) that communicate brain iron needs to endothelial cells in order to modulate iron transport.