目的 探讨血浆细胞周期依赖性激酶9（CDK9）水平与大动脉粥样硬化（LAA）型脑梗死病情进展及预后的相关性，评估其作为疾病风险分层及预后评估生物标志物的临床价值。方法 选取2020年1月—2024年12月期间于本院就诊的400例急性LAA型脑梗死患者作为观察组，并同期纳入100名健康体检者作为对照组。发病90 d后，采用改良Rankin量表（mRS）对所有患者进行预后评估。根据评估结果，将观察组进一步划分为预后不良组（152例）与预后良好组（248例）。检测患者血浆CDK9水平并收集临床资料。分析CDK9水平与美国国立卫生研究院卒中量表（NIHSS）评分、梗死灶体积的相关性；分析预后不良的影响因素。结果 观察组CDK9水平高于对照组［（185.6±42.3） pg/mL vs （62.4±18.5） pg/mL，P＜0.001］，且与梗死体积（r=0.586）、NIHSS评分（r=0.628）、高敏C反应蛋白（r=0.452）及白介素6（r=0.418）呈正相关（均P＜0.001）。多因素Logistic回归分析显示，CDK9升高是90天预后不良的独立危险因素。受试者工作特征曲线（ROC）曲线分析显示，CDK9预测预后不良的曲线下面积（AUC）为0.854（最佳截断值为198.6 pg/mL，灵敏度为78.3%，特异度为82.5%），联合NIHSS评分及梗死体积后AUC提升至0.912（P＜0.001）。结论 血浆CDK9水平可作为急性LAA型脑梗死病情进展及预后的独立预测标志物，联合传统指标可提高预后评估效能。

      Objective To investigate the correlation between plasma cyclin-dependent kinase 9（CDK9）level and disease progression and prognosis in patients with acute large artery atherosclerosis（LAA）cerebral infarction，and to evaluate its clinical value as a biomarker for disease risk stratification and prognostic assessment．Methods This study enrolled 400 patients with acute LAA-type cerebral infarction who visited our hospital between January 2020 and December 2024 as the observation group，along with 100 healthy individuals as the control group during the same period．After 90 days of symptom onset，all patients were assessed using the modified Rankin Scale（mRS）for prognostic evaluation．Based on the assessment results，the observation group was further divided into two subgroups：the poor prognosis group（152 cases）and the good prognosis group（248 cases）．Plasma CDK9 levels were measured，and clinical data were collected．The correlation between CDK9 level and National Institutes of Health Stroke Scale（NIHSS）score and infarct volume，and the factors affecting poor prognosis were analyzed．Results Plasma CDK9 levels in the observation group were higher than those in the control group（［185.6±42.3］ pg/mL vs ［62.4±18.5］ pg/mL，P＜0.001），and were positively correlated with infarct volume（r=0.586），NIHSS score（r=0.628），high-sensitivity C-reactive protein（r=0.452），and interleukin-6（r=0.418）（all P＜0.001）．Multivariate Logistic regression analysis showed that elevated CDK9 level was an independent risk factor for poor prognosis at 90 d．Receiver Operating Characteristic（ROC）curve analysis revealed that the area under the curve（AUC）of CDK9 for predicting poor prognosis was 0.854（optimal cut-off value：198.6 pg/mL，sensitivity：78.3%，specificity：82.5%），and the AUC increased to 0.912 when combined with NIHSS score and infarct volume（P＜0.001）．Conclusions Plasma CDK9 level may serve as an independent predictive biomarker for disease progression and prognosis in acute LAA cerebral infarction，and combining it with traditional indicators can improve the efficacy of prognostic assessment．

帕金森病（PD）是一种常见的与年龄相关的神经退行性疾病,其特点是黑质致密部内多巴胺能神经元的进行性丢失以及路易小体的积累。多巴胺能神经元的退化导致纹状体的多巴胺水平降低,最终出现静息性震颤、运动迟缓、肌肉僵硬和姿势不稳等运动症状,以及认知能力下降、嗅觉功能受损、精神异常和睡眠障碍等非运动症状。由于人口结构转变和全球老龄化,PD的不断增加对患者、家庭和社会构成重大负担。尽管广泛的研究已阐明了PD的病因学和潜在机制,但现有治疗主要集中在症状管理,无法阻止疾病的进展。小胶质细胞作为脑内重要的免疫细胞,对维持中枢神经系统的稳态具有关键作用。本文综述了PD研究,包括其病因学因素、分子机制和现有治疗策略。此外,审视了在PD样模型中涉及小胶质细胞的研究,深入探讨了小胶质细胞在疾病进展中的动态,并探究了小胶质细胞在促进或减轻疾病进展方面所扮演的错综角色。通过这样的探讨,本综述旨在为PD复杂的发病机制提供新的洞见和观点,激发出针对性治疗干预的创新思路。

Parkinson's disease（PD）,a prevalent age-related neurodegenerative disorder,is characterized by the progressive loss of dopaminergic neurons within the substantia nigra compacta（SNc）and the accumulation of Lewy bodies．The degeneration of dopaminergic neurons leads to diminished striatal dopamine levels,culminating in motor symptoms such as resting tremors,bradykinesia,muscle rigidity and postural instability,alongside non-motor manifestations encompassing cognitive decline,impaired olfactory function,psychological abnormalities and sleep disturbances．The escalating incidence of PD due to shifting demographics and global aging poses substantial burdens on patients,families and society．Although extensive research has elucidated the etiology and underlying mechanisms of PD,available treatments largely focus on symptom management and lack the capacity to halt disease progression．Microglia,as integral immune cells within the brain,wield pivotal influence over central nervous system homeostasis．This review presents a comprehensive synthesis of PD,encompassing its etiological factors,molecular mechanisms,and existing therapeutic strategies．Furthermore,we scrutinized research involving microglia in PD-like models,delving into the dynamics of microglia in disease progression and probing into the intricate roles that microglia assume in either fostering or mitigating disease advancement．By doing so,this review aims to furnish novel insights and perspectives that shed light on the intricate pathogenesis of PD,potentially sparking innovative concepts for targeted therapeutic interventions．