ArticleFrontiers in molecular neuroscience2024
Post-translational modifications of beta-amyloid alter its transport in the blood-brain barrier
Article in Frontiers in molecular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Construction and Applicability Scenarios of 3D Neurovascular Unit Models In Vitro.Biomolecules · 2026Review
- Magnetoreceptive CRY/MagR complexes: linking circadian redox signalling to protein aggregation in Alzheimer's and Parkinson's disease.ADMET & DMPK · 2026Review
- The Tetrapeptide HAEE Promotes Amyloid-Beta Clearance from the Brain.International journal of molecular sciences · 2025Article
- Therapeutic Potential of HAEEPGP Peptide Against β-Amyloid Induced Neuropathology.Molecular neurobiology · 2025Article
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Short-Term Inhibition of NOX2 Prevents the Development of Aβ-Induced Pathology in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Biophysical insights into the molecular mechanisms of beta amyloid aggregation and its toxic effects in Alzheimer's disease.Frontiers in molecular biosciences · 2025Review
- Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 Aβ
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