Post-translational modifications of beta-amyloid alter its transport in the blood-brain barrier in vitro model.

ABSTRACT: One of the hallmarks of Alzheimer's disease (AD) is the accumulation of beta-amyloid peptide (Aβ) leading to formation of soluble neurotoxic Aβ oligomers and insoluble amyloid plaques in various parts of the brain. Aβ undergoes post-translational modifications that alter its pathogenic properties. Aβ is produced not only in brain, but also in the peripheral tissues. Such Aβ, including its post-translationally modified forms, can enter the brain from circulation by binding to RAGE and contribute to the pathology of AD. However, the transport of modified forms of Aβ across the blood-brain barrier (BBB) has not been investigated. Here, we used a transwell BBB model as a controlled environment for permeability studies. We found that Aβ₄₂ containing isomerized Asp7 residue (iso-Aβ

SUBMITTER: Varshavskaya KB 

PROVIDER: S-EPMC10954796 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature