A number of mechanisms may be at play including decreased plasma iron due to abnormal transferrin desaturation (Hare et al., 2015) and increased levels of oxidized hemoglobin and heme which abnormally bind and colocalize with amyloid-beta senile plaques causing cerebral amyloid angiopathy (Perry et al., 2008; Chuang et al., 2012). The gene discussed is TF; the disease is cerebral amyloid angiopathy.