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REVIEW article

Front. Aging Neurosci.
Sec. Parkinson’s Disease and Aging-related Movement Disorders
Volume 16 - 2024 | doi: 10.3389/fnagi.2024.1451655
This article is part of the Research Topic Common pathophysiology underpinning Parkinson's disease and other neurodegenerative diseases View all 12 articles

Primary cilia in Parkinson's disease: summative roles in signaling pathways, genes, defective mitochondrial function and substantia nigra dopaminergic neurons

Provisionally accepted
Zijiao Tian Zijiao Tian Yixin Zhang Yixin Zhang Jing Xu Jing Xu Qianwen Yang Qianwen Yang Die Hu Die Hu Jing Feng Jing Feng *Cong Gai Cong Gai *
  • Beijing University of Chinese Medicine, Beijing, China

The final, formatted version of the article will be published soon.

    Primary cilia (PC) are microtubules-based, independent antennal-like sensory organelles, that are seen in most vertebrate cells of different types, including astrocytes and neurons. They send signals to cells to control many physiological and cellular processes by detecting changes in the extracellular environment. Parkinson's disease (PD), a neurodegenerative disease that progresses over time, is primarily caused by a gradual degradation of the dopaminergic pathway in the striatum nigra, which results in a large loss of neurons in the substantia nigra compact (SNpc) and a depletion of dopamine (DA). PD samples have abnormalities in the structure and function of PC. The alterations contribute to the cause, development, and recovery of PD via influencing signaling pathways (SHH, Wnt, Notch-1, α-syn, and TGFβ), genes (MYH10 and LRRK2), defective mitochondrial function, and substantia nigra dopaminergic neurons. Thus, restoring the normal structure and physiological function of PC and neurons in the brain are effective treatment for PD. This review summarizes the function of PC in neurodegenerative diseases and explores the pathological mechanisms caused by PC alterations in PD, in order to provide references and ideas for future research.

    Keywords: primary cilia, Parkinson's disease, signaling pathway, gene, defective mitochondrial function, substantia nigra dopaminergic neuron

    Received: 19 Jun 2024; Accepted: 02 Sep 2024.

    Copyright: © 2024 Tian, Zhang, Xu, Yang, Hu, Feng and Gai. 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:
    Jing Feng, Beijing University of Chinese Medicine, Beijing, China
    Cong Gai, Beijing University of Chinese Medicine, Beijing, 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.