The role of human serum albumin in prevention and treatment of Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) has been and remains the main cause of dementia in aging patients. This neurodegenerative disease belongs to the progressive and socially significant ones. There are several hypotheses for the development of AD: the tau hypothesis, the amyloid cause, the cholinergic cause, the cause of oxidative stress and inflammation. The lack of a generally accepted understanding of the etiology and pathogenesis of AD hinders the development of new effective mechanisms for its treatment and prevention. In 2021, for the first time, a drug for pathogenetic therapy of AD (aducanumab) was approved, which helps to reduce the content of amyloid-β peptide (Aβ) in the brain of patients. Another promising approach to the treatment of AD, aimed at removing Aβ from the patient’s central nervous system, is the impact on human serum albumin (HSA), which carries 90% of Aβ in the blood serum and 40–90% of Aβ in the cerebrospinal fluid. In clinical practice, plasmapheresis has already been tested and shown to be effective with the replacement of one’s own HSA with a purified therapeutic albumin preparation. Another variant of this approach is to enhance the interaction of HSA with Aβ through the action of exogenous and endogenous HSA ligands, such as serotonin, ibuprofen and some unsaturated fatty acids. In vivo studies confirm the association of this group of ligands with the pathogenesis of AD. These substances are well-studied natural metabolites or drugs, which greatly simplifies the development of new methods of therapy and prevention of AD with their use. In general, a new direction of scientific research devoted to the study of HSA as a carrier and depot of Aβ in the blood and cerebrospinal fluid will expand our understanding of Aβ metabolism and its role in the pathogenesis of AD.