中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (7): 1491-1492.doi: 10.4103/1673-5374.361545

• 观点:退行性病与再生 • 上一篇    下一篇

阿尔茨海默病中的水通道蛋白5:口腔和大脑病理之间的联系?

  


  • 出版日期:2023-07-15 发布日期:2023-01-11

Aquaporin 5 in Alzheimer’s disease: a link between oral and brain pathology?

Cristina Municio*, Eva Carro*   

  1. Group of Neurodegenerative Diseases, Hospital Universitario 12 de Octubre Research Institute (imas12), Madrid, Spain (Municio C)
    Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain (Municio C, Carro E)
    Neurobiology of Alzheimer’s Disease Unit, Functional Unit for Research into Chronic Diseases, Instituto de Salud Carlos III, Madrid, Spain (Carro E)
  • Online:2023-07-15 Published:2023-01-11
  • Contact: Eva Carro, PhD, eva.carro@isciii.es; Cristina Municio, PhD, cmunicio.imas12@h12o.es.

摘要: https://orcid.org/0000-0002-6504-4579 (Eva Carro)
https://orcid.org/0000-0002-8552-8183 (Cristina Municio)

Abstract: The involvement of aquaporins (AQPs) in the development of diseases has been widely described (Azad et al., 2021). AQP5 has been described in astrocytes changing after traumatic brain injuries (Chai et al., 2013), but the precise role of AQP5 in Alzheimer’s disease (AD) pathology is yet to be understood. We have recently reported that AQP5 expression changes during the development of AD (Antequera et al., 2022). The AQP5 expression in salivary glands is decreased in 6-month-old APP/PS1 mice and AD patients. This decrease in AQP5 expression could be involved in the mechanism of salivary gland dysfunction described in a previous study (Antequera et al., 2021). Now, we propose a new indirect role of AQP5 in the connection between infection-induced oral dysbiosis and AD (Sureda et al., 2020). Here, we suggest that the proinflammatory response induced by oral pathogen infection results in the downregulation of AQP5 contributing to the salivary gland secretory dysfunction. All these alterations destabilize the peripheral immune-inflammatory balance and exacerbate neuroinflammation and neurodegeneration leading to AD pathology.