Aβ may be chelating copper ions away from the CNS via possible combined export across LRP1 (Wang et al., 2021), and or concurrently through direct sequestration of copper in the serum that would exit through urinary excretion, as abnormal Aβ levels and ratios are a common feature AD patients urine (Yang et al., 2021). Here, LRP1 is linked to Alzheimer disease.