中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (1): 127-128.doi: 10.4103/1673-5374.340407

• 观点:退行性病与再生 • 上一篇    下一篇

多发性硬化症的突触病理学:Nogo-A 信号在星形胶质细胞中的作用?

  

  • 出版日期:2023-01-15 发布日期:2022-06-17

Synaptic pathology in multiple sclerosis: a role for Nogo-A signaling in astrocytes?

Sheila Espírito-Santo*, Vinícius Gabriel Coutinho, Flávia Carvalho Alcantara Gomes   

  1. Laboratório de Biologia Celular e Tecidual, Universidade Estadual do Norte Fluminense Darcy Ribeiro, Campos dos Goytacazes, RJ, Brazil (Espírito-Santo S)
    Laboratório de Neurobiologia Celular, Universidade Federal do Rio de Janeiro, Instituto de Ciências Biomédicas, Rio de Janeiro, RJ, Brazil (Coutinho VG, Gomes FCA)
  • Online:2023-01-15 Published:2022-06-17
  • Contact: Sheila Espírito-Santo, PhD, espiritosanto.sheila@gmail.com
  • Supported by:
    Work in the laboratories of the authors was supported by grants from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) (to FCAG and VGC), Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) (to FCAG), and Ministério da Saúde (MS-Decit) (to FCAG). 

摘要: https://orcid.org/0000-0001-8359-3435 (Sheila Espírito-Santo)

Abstract: Multiple sclerosis (MS) is characterized as an inflammatory demyelinating disease that affects the central nervous system (CNS), leading to sensory, motor and cognitive impairments. Ultimately, axonal denudation culminates in axonal lesions and neurodegeneration. Inflammatory demyelinating lesions in MS are associated with infiltration of immune cells combined with activation of the resident CNS inflammatory cells, astro- and microglia. Recently, synaptopathy has been associated with MS pathophysiology, though, intriguingly, it can occur independently of demyelination (Jürgens et al., 2016). Although inflammation also seems to corroborate with synaptic abnormalities, associated or not with demyelinating lesions, the underlying mechanisms are not fully understood (Mandolesi et al., 2015). In the last decades, the myelin inhibitory protein neurite outgrowth inhibitor-A (Nogo-A) has emerged as a potential mediator of axonal and synaptic dysfunctions in MS and a promising target to be neutralized  (Ineichen et al., 2017). Based on our recent findings demonstrating that Nogo-A signaling regulates astrocyte-driven synaptogenesis (Espírito-Santo et al., 2021),  and considering the critical role of astrocytes in regulating synaptic plasticity and function (Allen and Eroglu, 2017), we propose that modulation of Nogo-A pathway in these cells is a new mechanism driving circuitry alterations of MS.