Abstract：
Post-stroke depression (PSD) is one of the most common mental sequelae after a stroke and can damage the brain. Although PSD has garnered increasing attention in recent years, the precise mechanism remains unclear. Studies have indicated that the expression of DAPK1 is elevated in various neurodegenerative conditions, including depression, ischemic stroke, and Alzheimer\'s disease. However, the specific molecular mechanism of DAPK1-mediated cognitive dysfunction and neuronal apoptosis in PSD rats is unclear. In this study, we established a rat model of PSD, and then assessed depression-like behaviors and cognitive dysfunction in rats using behavioral tests. In addition, we detected neuronal apoptosis and analyzed the expression of DAPK1 protein and proteins related to the ERK/CREB/BDNF signaling pathway. The findings revealed that MCAO combined with CUMS can induce more severe depression-like behaviors and cognitive dysfunction in rats, while overexpression of DAPK1 may hinder the downstream ERK/CREB/BDNF signaling pathways, resulting in neuronal loss and exacerbation of brain tissue damage. In this study, we will focus on DAPK1 and explore its role in PSD.
摘要：
卒中后抑郁（PSD）是中风后最常见的精神后遗症之一，可损害大脑。尽管PSD近年来受到越来越多的关注，确切机制尚不清楚.研究表明，DAPK1的表达在各种神经退行性疾病中升高，包括抑郁症,缺血性卒中,和老年痴呆症。然而,DAPK1介导PSD大鼠认知功能障碍和神经元凋亡的具体分子机制尚不清楚。在这项研究中,建立了PSD大鼠模型,然后使用行为测试评估大鼠的抑郁样行为和认知功能障碍。此外,检测神经细胞凋亡,分析DAPK1蛋白及ERK/CREB/BDNF信号通路相关蛋白的表达。提示MCAO联合CUMS可诱发大鼠更严重的抑郁样行为和认知功能障碍,而DAPK1的过表达可能会阻碍下游的ERK/CREB/BDNF信号通路，导致神经元丢失和脑组织损伤加剧。在这项研究中,我们将重点关注DAPK1并探讨其在PSD中的作用。
