REVIEW article
Front. Cell Dev. Biol.
Sec. Membrane Traffic and Organelle Dynamics
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1650884
This article is part of the Research TopicProtein Trafficking to the Primary Cilium: Molecular Pathways and Clinical ImplicationsView all 3 articles
Primary Cilia in the Mature Brain: Emerging Roles in Alzheimer's Disease Pathogenesis
Provisionally accepted- 1Department of Chemistry, Hong Kong Baptist University, Hong Kong, Hong Kong, SAR China
- 2Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
- 3Consun Chinese Medicines Research Centre for Renal Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, Hong Kong, SAR China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Primary cilia are microtubule-based structures that resemble antennae and function as sensory organelles. Dysfunction of primary cilia has been linked to various age-related conditions. Alzheimer's disease, which affects more than 38.5 million individuals worldwide, is a prominent neurodegenerative disorder, with aging being its most significant risk factor. In this review, we provide an overview of current findings on the role of primary cilia in the mature brain and the mechanisms by which alteration of primary cilia may influence the progression of Alzheimer's disease. Growing evidence reveals that primary cilia in the mature brain play dynamic roles in cell type, region, and age-dependent manners. In Alzheimer's disease, anomalies in primary cilia functions and morphology are closely associated with key pathologies. However, the exact mechanisms remain unclear. Future studies on neuronal and glial cilia dynamics during aging and neurodegeneration are essential to explore their potential as therapeutic targets.
Keywords: primary cilia, Alzheimer's disease, Pathogenesis, G protein-coupled receptors, AβPlaques
Received: 20 Jun 2025; Accepted: 05 Sep 2025.
Copyright: © 2025 Huang, Li and HOR. 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: Catherine Hong Huan HOR, Department of Chemistry, Hong Kong Baptist University, Hong Kong, Hong Kong, SAR China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.