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

被引：1
|
作者：
Piacentini, Roberto [1 ,2 ]
Grassi, Claudio [1 ,2 ]
机构：
[1] Univ Cattolica Sacro Cuore, Dept Neurosci, Rome, Italy
[2] Fdn Policlin Univ A Gemelli, IRCCS, Rome, Italy
来源：
NEURAL REGENERATION RESEARCH | 2025年 / 20卷 / 02期
关键词：
herpes simplex virus type 1; interleukin; 1; beta; microglia; neuroinflammation; synaptic dysfunction; HIPPOCAMPAL NEURON MORPHOLOGY; ALZHEIMERS-DISEASE; TNF-ALPHA; PULMONARY INFLAMMATION; DUAL ROLE; ASTROCYTES; NEUROINFLAMMATION; PLASTICITY; IL-1-BETA; CYTOKINES;
D O I：
10.4103/NRR.NRR-D-23-01690
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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 1 beta as a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.
引用
收藏
页码：416 / 423
页数：8
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