The imbalance between the production and clearance of β-amyloid peptide (Aβ) from the central nervous system (CNS) is a key factor in pathogenesis of Alzheimer's disease (AD). Human serum albumin (HSA), as a depot of Aβ in the peripheral blood, favors clearance of Aβ from the CNS. HSA carries a variety of ligands that have the potential to affect the HSA-Aβ interaction. Similarly, this interaction can be modulated by Aβ ligands. In our work, we studied the influence of a number of low-molecular-weight ligands of HSA, as well as some regulatory neuroinflammatory proteins with affinity for Aβ, on HSA interaction with monomeric form of Aβ. The established in vitro effects are consistent with clinical data and those obtained in animal models, demonstrating the applicability of our approach in developing new compounds for AD treatment and prevention.
Shevelyova et al. (Sun,) studied this question.