中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (8): 1649-1650.doi: 10.4103/1673-5374.389645

• 观点:退行性病与再生 • 上一篇    下一篇

p38 MAPK和CDK5,神经炎症的信号通路:阿尔茨海默病的潜在治疗干预?

  

  • 出版日期:2024-08-15 发布日期:2024-01-03

p38-MAPK and CDK5, signaling pathways in neuroinflammation: a potential therapeutic intervention in Alzheimer’s disease?

Vlad Ionut Viorel, Ylenia Pastorello, Nosherwan Bajwa, Mark Slevin*   

  1. George Emil Palade University of Medicine, Pharmacy, Science and Technology, Târgu Mures, Romania (Viorel VI) 
    Department of Anatomy and Embryology, George Emil Palade University of Medicine, Pharmacy, Science and Technology, Târgu Mures, Romania (Pastorello Y) 
    DIAKO Hospital, Flensburg, Germany (Bajwa N) 
    Center for Advanced Medical and Pharmaceutical Research (CCAMF), George Emil Palade University of Medicine, Pharmacy, Science and Technology, Târgu Mures, Romania (Slevin M) 
    Manchester Metropolitan University, Manchester, UK (Slevin M) 
  • Online:2024-08-15 Published:2024-01-03
  • Contact: Mark Slevin, PhD, mark.slevin@umfst.ro.

摘要: https://orcid.org/0000-0003-3767-4861 (Mark Slevin)

Abstract: Alzheimer’s disease (AD), the most common type of dementia, affects millions of people worldwide, putting a significant strain on healthcare infrastructure and societal resources. AD is characterized by the build-up of amyloid-beta (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. These pathological features cause neuroinflammation, vascular dysfunction, and ultimately, neuronal death and cognitive decline (Long and Holtzman, 2019). Two critical signaling pathways, the mitogen-activated protein kinase (MAPK) family and cyclin-dependent kinase 5 (CDK5), have been implicated in the pathogenesis of AD. There are three primary subfamilies within the MAPK family, namely extracellular signal-regulated kinases, c-Jun N-terminal kinases, and p38 MAPKs. Of these, p38α MAPK is particularly involved in neuroinflammation and vascular dysfunction, processes that are integral to the progression of AD. CDK5, a serine/threonine kinase primarily expressed in the central nervous system, has crucial roles in neuronal migration, synapse formation, and synaptic plasticity. However, aberrant activation of CDK5 has been linked to various neurodegenerative diseases, including AD.