突触可塑性
神经科学
机制(生物学)
认知
病态的
神经可塑性
可塑性
疾病
变质塑性
医学
心理学
病理
内科学
物理
哲学
认识论
热力学
受体
作者
Lin Yang,Jin Li,Fuhong Liu,Xin Chai,Zongping Fang,Xijing Zhang
出处
期刊:Current Neuropharmacology
[Bentham Science]
日期:2024-10-28
卷期号:23
标识
DOI:10.2174/1570159x23666241028105746
摘要
Sepsis-associated encephalopathy (SAE) is a form of cognitive and psychological impairment resulting from sepsis, which occurs without any central nervous system infection or structural brain injury. Patients may experience long-term cognitive deficits and psychiatric disorders even after discharge. However, the underlying mechanism remains unclear. As cognitive function and mental disease are closely related to synaptic plasticity, it is presumed that alterations in synaptic plasticity play an essential role in the pathological process of SAE. Here, we present a systematic description of the pathogenesis of SAE, which is primarily driven by glial cell activation and subsequent release of inflammatory mediators. Additionally, we elucidate the alterations in synaptic plasticity that occur during SAE and comprehensively discuss the roles played by glial cells and inflammatory factors in this process. In this review, we mainly discuss the synaptic plasticity of SAE, and the main aim is to show the consequences of SAE on inflammatory factors and how they affect synaptic plasticity. This review may enhance our understanding of the mechanism underlying cognitive dysfunction and provide valuable insights into identifying appropriate therapeutic targets for SAE.
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