Pathology of Amyloid-β (Aβ) Peptide Peripheral Clearance in Alzheimer’s Disease
Tsoy A. Umbayev B. Kassenova A. Kaupbayeva B. Askarova S.
October 2024Multidisciplinary Digital Publishing Institute (MDPI)
International Journal of Molecular Sciences
2024#25Issue 20
Although Alzheimer’s disease (AD) is traditionally viewed as a central nervous system disorder driven by the cerebral accumulation of toxic beta-amyloid (Aβ) peptide, new interpretations of the amyloid cascade hypothesis have led to the recognition of the dynamic equilibrium in which Aβ resides and the importance of peripheral Aβ production and degradation in maintaining healthy Aβ levels. Our review sheds light on the critical role of peripheral organs, particularly the liver, in the metabolism and clearance of circulating Aβ. We explore the mechanisms of Aβ transport across the blood–brain barrier (BBB) via transport proteins such as LRP1 and P-glycoprotein. We also examine how peripheral clearance mechanisms, including enzymatic degradation and phagocytic activity, impact Aβ homeostasis. Our review also discusses potential therapeutic strategies targeting peripheral Aβ clearance pathways. By enhancing these pathways, we propose a novel approach to reducing cerebral Aβ burden, potentially slowing AD progression.
Alzheimer’s disease , amyloid-β peptide , enzymatic degradation , peripheral clearance
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Center for Life Sciences, National Laboratory Astana, Nazarbayev University, Astana, 010000, Kazakhstan
Faculty of Natural Sciences, Eurasian National University, Astana, 010000, Kazakhstan
Center for Life Sciences
Faculty of Natural Sciences
10 лет помогаем публиковать статьи Международный издатель
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