2019 年冠状病毒病 (COVID-19) 可导致神经系统症状，例如头痛、意识模糊、癫痫发作、听力丧失和嗅觉丧失。 COVID-19与帕金森病（PD）之间的联系正在调查中，但需要更多的研究来确定明确的联系。选择数据集GSE22491和GSE164805来筛选差异表达基因（DEG），并进行免疫浸润和基因集富集分析（进行了 DEG 的 GSEA）。 WGCNA 分析了 DEG 并选择了交叉基因。确定潜在的生物学功能和信号通路，并利用基因表达和受试者工作特征（ROC）曲线进一步筛选诊断基因。布洛芬作为治疗靶点的筛选和分子对接。通过构建体外PD模型，构建“COVID19-PD”信号通路，探索血管紧张素转换酶2（ACE2）在PD中的作用，验证了布洛芬的有效性。从GSE36980中筛选出13个DEG和 GSE5281 数据集。京都基因与基因组百科全书（KEGG）分析显示，DEG主要与缺氧诱导因子（HIF-1）、表皮生长因子受体（EGFR）酪氨酸激酶抑制剂耐药等相关。经分析发现：布洛芬通过抑制核因子 kappa-B (NF-κB)、白介素-1β (IL-1β)、IL-6 和肿瘤坏死因子-α (TNF-α) 的表达来缓解 PD 症状。基于信号通路构建，ACE2 在 COVID-19 诱导的 PD 中的重要性已被确​​定。 ACE2被发现在大脑中广泛分布。在 1-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 诱导的 ACE2 缺失 PD 小鼠模型中，运动和非运动症状更严重，NF-κB p65 和 α- 增加突触核蛋白 (α-syn) 表达显着聚集、酪氨酸羟化酶 (TH) 减少、严重神经元丢失和神经退行性疾病。严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染通过炎症环境和增加 PD 风险ACE2 下调，为与 COVID-19 和 PD 相关的分子机制和靶向治疗提供证据。© 2024 Liu 等人。

The coronavirus disease 2019 (COVID-19) can lead to neurological symptoms such as headaches, confusion, seizures, hearing loss, and loss of smell. The link between COVID-19 and Parkinson's disease (PD) is being investigated, but more research is needed for a definitive connection.Datasets GSE22491 and GSE164805 were selected to screen differentially expressed gene (DEG), and immune infiltration and gene set enrichment analysis (GSEA) of the DEG were performed. WGCNA analyzed the DEG and selected the intersection genes. Potential biological functions and signaling pathways were determined, and diagnostic genes were further screened using gene expression and receiver operating characteristic (ROC) curves. Screening and molecular docking of ibuprofen as a therapeutic target. The effectiveness of ibuprofen was verified by constructing a PD model in vitro, and constructing "COVID19-PD" signaling pathway, and exploring the role of angiotensin-converting enzyme 2 (ACE2) in PD.A total of 13 DEG were screened from the GSE36980 and GSE5281 datasets. Kyoto encyclopedia of genes and genomes (KEGG) analysis showed that the DEG were mainly associated with the hypoxia-inducible factor (HIF-1), epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance, etc. After analysis, it is found that ibuprofen alleviates PD symptoms by inhibiting the expression of nuclear factor kappa-B (NF-κB), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). Based on signal pathway construction, the importance of ACE2 in COVID-19-induced PD has been identified. ACE2 is found to have widespread distribution in the brain. In the 1-methyl-4-phenyl-1,2,3,6-te-trahydropyridine (MPTP)-induced ACE2-null PD mice model, more severe motor and non-motor symptoms, increased NF-κB p65 and α-synuclein (α-syn) expression with significant aggregation, decreased tyrosine hydroxylase (TH), severe neuronal loss, and neurodegenerative disorders.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection increases the risk of PD through an inflammatory environment and downregulation of ACE2, providing evidence for the molecular mechanism and targeted therapy associated with COVID-19 and PD.© 2024 Liu et al.