The Aβ-buffering role of HSA could be exploited for AD therapy by directed improvement of HSA’s affinity to Aβ, as exemplified by the addition of certain low-molecular-weight ligands of HSA: arachidonic/linoleic acid or serotonin (the maximal effect is a 17-fold increase in HSA’s affinity to Aβ [12,13]). Here, ALB is linked to Alzheimer disease.