中国神经再生研究(英文版) ›› 2024, Vol. 20 ›› Issue (2): 416-423.doi: 10.4103/NRR.NRR-D-23-01690

• 综述:退行性病与再生 • 上一篇    下一篇

白细胞介素1β受体与1型单纯疱疹病毒复发性脑感染的突触功能障碍

  

  • 出版日期:2025-02-15 发布日期:2024-06-18

Interleukin 1β receptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1

Roberto Piacentini1, 2, *, Claudio Grassi1, 2   

  1. 1Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy; 2Fondazione Policlinico Universitario A. Gemelli, IRCCS, Rome, Italy
  • Online:2025-02-15 Published:2024-06-18
  • Contact: Roberto Piacentini, PhD, roberto.piacentini@unicatt.it.
  • Supported by:
    This work was supported by Università Cattolica (D1 intramural funds to RP) and by Italian Ministry of University and Research (PRIN 2022ZYLB7B and P2022YW7BP funds to CG).

摘要: https://orcid.org/0000-0003-4215-1643 (Roberto Piacentini)

Abstract: Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease. However, the molecular mechanisms underlying this association are not completely understood. Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role. Here, we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain, highlighting the role of interleukins and, in particular, interleukin 1β as a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.

Key words: herpes simplex virus type 1, interleukin 1β, microglia, neuroinflammation, synaptic dysfunction