BRIEF RESEARCH REPORT article
Front. Cell. Neurosci.
Sec. Cellular Neuropathology
This article is part of the Research TopicHuman Brain Organoids: From Seeding to Analysis. Proceeding From the Brain Organoids Summer School BOSS25View all articles
Choroid plexus organoids mimic amyloid uptake at the blood-cerebrospinal fluid-barrier
Provisionally accepted
Cristina Municio1,2*
Kyriaki Sapidou3
Elizabeth J Apsley3
Marian Fernandez-Otero3
Charlie Edward Arber4
Selina Wray4
Eva Carro1,2
Laura Pellegrini3*- 1Neurobiology of Alzheimer´s disease Unit, Instituto de Salud Carlos III, Madrid, Spain
- 2Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas, Madrid, Spain
- 3Centre for Developmental Neurobiology, King's College London, London, United Kingdom
- 4Department of Neurodegenerative Disease, Queen Square Institute of Neurology, University College London, London, United Kingdom
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The choroid plexus (ChP) is a specialised tissue of the central nervous system that produces cerebrospinal fluid (CSF), maintains cerebral homeostasis and forms the blood-CSF barrier (B-CSF-B), a key interface that regulates the exchange of substances between the blood and the brain. Despite its physiological importance, the involvement of the ChP in neurodegenerative diseases such as Alzheimer's disease (AD), remains poorly understood. This is largely due to the reliance on murine models and the limited availability of human brain tissue. Recent advances in human stem-cell derived ChP organoids now offer a more physiologically relevant model to interrogate ChP role in human health and disease. Given that in AD pathology beta-amyloid (Aβ) accumulation has been linked to early disruption of brain barriers, studying the B-CSF-B is particularly relevant. Transthyretin (TTR), the predominant protein secreted by the ChP, is thought to play a role in the transport and clearance of Aβ, although its exact mechanisms are not yet fully elucidated. Here, we propose the use of ChP organoids to investigate the role of the B-CSF-B in amyloid uptake which may contribute to barrier dysfunction and disease progression in AD.
Keywords: Alzheimer Disease, Amyloid - beta, Cerebrospinal fluid barrier (BCSFB), Choroid plexus (CP), Organoid
Received: 17 Dec 2025; Accepted: 27 Jan 2026.
Copyright: © 2026 Municio, Sapidou, Apsley, Fernandez-Otero, Arber, Wray, Carro and Pellegrini. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Cristina Municio
Laura Pellegrini
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