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通过改善神经炎症和树突损失,eIF4E酸化介导的LPS诱导了类似抑郁的行为

Qichao Gong¹, Weifen Li^1,2, Tahir Ali¹

¹State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, Guangdong, China.

Translational psychiatry

|November 17, 2023

概括

神经炎症通过通过eIF4E和TrkB/BDNF信号来破坏突触蛋白质合成,导致类似抑郁症的症状. 用eFT508治疗逆转了这些影响,突出了治疗干预的关键途径.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

翻译缺陷在神经疾病中很常见,与突触异常和抑郁症有关.
涉及到4E真核启动因子 (eIF4E) 和热胺受体激酶B (TrkB) /脑衍生神经营养因子 (BDNF) 信号的改变.

研究的目的:

调查eIF4E在脂聚糖 (LPS) 诱导的神经炎症和抑郁症中的作用.
为了确定eIF4E失调是否与通过TrkB/BDNF通路的突触蛋白质损失相关.

主要方法:

使用动物行为测试,生化分析和药理干预措施.
在动物模型中,LPS被用来诱导神经炎症和类似抑郁的行为.
评估了eIF4E抑制剂eFT508和TrkB抗剂K252a的作用.

主要成果:

使用LPS诱导了抑郁行为,神经炎症,脊柱密度降低和突触蛋白质失调.
LPS增强了eIF4E酸化和受损了TrkB/BDNF信号传递.
eFT508治疗改善了LPS诱导的影响,恢复了突触蛋白,并使eIF4E和TrkB/BDNF信号正常化.

结论:

在炎症相关抑郁症中,eIF4E介导的翻译失调会通过TrkB/BDNF通路导致突触蛋白损失.
针对eIF4E和TrkB/BDNF信号传递,代表了神经炎症性抑郁症的潜在治疗策略.

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Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.