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目的 观察脑梗死后认知功能障碍患者血清γ分泌酶水平变化，分析血清γ分泌酶水平对脑梗死后发生认知功能障碍的预测价值，并观察梗死部位。方法 选取2021年6月—2024年5月贵州省第二人民医院收治的脑梗死患者114例，使用简易智能状态量表（MMSE）对脑梗死患者进行评估，根据评估结果将114例患者分为认知功能障碍组（54例，MMSE评分<27分）和认知功能正常组（60例，MMSE评分≥27分），采用ELISA法检测血清γ分泌酶，绘制受试者工作特征曲线，分析血清γ分泌酶水平对脑梗死后发生认知功能障碍的预测价值，另观察梗死部位。结果 认知功能障碍组及认知功能正常组血清γ分泌酶水平分别为（906.63±271.60）、（627.26±254.38）pg/mL，两组比较，P<0.05。血清γ分泌酶水平预测脑梗死后认知功能障碍的AUC为0.783(95%CI:0.698～0.867)，当最佳截断值为722.79 pg/mL时，其预测灵敏度和特异度分别为0.833、0.650。认知功能障碍组梗死部位累及额叶21例（38.89%）、累及其他部位33例（61.11%），认知功能正常组分别为11例（18.33%）、49例（81.67%），两组比较，P均<0.05。结论 血清γ分泌酶水平在脑梗死患者中升高，其对脑梗死后认知功能障碍具有一定的预测价值；当梗死部位为额叶时，可能更易出现认知功能障碍。
Abstract：Objective To observe the changes in serum γ-secretase levels in patients with cognitive dysfunction following cerebral infarction, to analyze the predictive value of serum γ-secretase levels for the occurrence of cognitive dysfunction after cerebral infarction, and to examine the locations of the infarction. Methods A total of 114 patients with cerebral infarction admitted to the Second People's Hospital of Guizhou Province from June 2021 to May 2024 were selected, and we evaluated the patients with cerebral infarction using the Mini-Mental State Examination(MMSE), and then the 114 patients were divided into the cognitive dysfunction group(54 cases, MMSE score < 27 points) and normal cognitive function group(60 cases, MMSE score ≥ 27 points). The serum γ-secretase was detected by ELISA, and the receiver operating characteristic(ROC) curve was plotted. The predictive value of serum γ-secretase level on cognitive dysfunction after cerebral infarction was analyzed, and the infarct location was observed. Results The serum γ-secretase levels in the cognitive dysfunction group and the normal cognitive function group were(906. 63 ± 271. 60) and(627. 26 ± 254. 38) pg/mL, respectively, with statistically significant difference between the two groups(P<0. 05). The AUC of serum γ-secretase level in predicting cognitive dysfunction after cerebral infarction was 0. 783(95% CI: 0. 698-0. 867), and the sensitivity and specificity were 0. 833 and 0. 650, respectively, when the optimal cut-off value was 722. 79 pg/mL. In the group with cognitive functional impairment, there were 21 cases(38. 89%) with infarction locations involving the frontal lobe and 33 cases(61. 11%) involving other regions. In the group with normal cognitive function, there were 11 cases(18. 33%) and 49 cases(81. 67%) respectively; there were significant differences between the two groups(all P<0. 05). Conclusion The serum γ-secretase level increases in patients with cerebral infarction, which has a certain predictive value for cognitive dysfunction after cerebral infarction. When the infarct location is the frontal lobe, cognitive impairment may be more likely to occur.
[1] CHEN Z L, LI Q, YANG J Y, et al. The prevalence and risk factors of posttraumatic cerebral infarction in patients with traumatic brain injury:a systematic review and metaanalysis[J]. Bioengineered, 2022,13(5):11706-11717.
[2] WEN H, LV M. Correlation analysis between serum procalcitonin and infarct volume in young patients with acute cerebral infarction[J]. Neurol Sci, 2021,42(8):3189-3196.
[3] ZENG Q, HUANG Z, WEI L, et al. Correlations of serum cystatin C level and gene polymorphism with vascular cognitive impairment after acute cerebral infarction[J]. Neurol Sci, 2019,40(5):1049-1054.
[4] YE B, WEI D, PAN L. Montreal cognitive assessment of cognitive dysfunction after basal ganglia stroke[J]. Acta Neurol Belg,2022,122(4):881-884.
[5] MIJAJLOVIC M D, PAVLOVIC A, BRAININ M, et al. Poststroke dementia-a comprehensive review[J]. BMC Med, 2017,15(1):11.
[6] ZHAO L, BIESBROEK J M, SHI L, et al. Strategic infarct location for post-stroke cognitive impairment:a multivariate lesionsymptom mapping study[J]. J Cereb Blood Flow Metab, 2018,38(8):1299-1311.
[7] LEI C Y, DENG Q H, LI H J, et al. Association between silent brain infarcts and cognitive function:a systematic review and meta-analysis[J]. J Stroke Cerebrovasc Dis, 2019,28(9):2376-2387.
[8]中国中西医结合学会神经科专业委员会.中国脑梗死中西医结合诊治指南（2017）[J].中国中西医结合杂志，2018,38(2):136-144.
[9]杜志刚，王宇，伊红丽，等.术前双重抗血小板治疗对Solumbra机械取栓急性脑梗死患者神经功能及血流动力学的影响[J].中国实用神经疾病杂志，2023,26(1):1-6.
[10] FINNEY C A, MORRIS M J, WESTBROOK R F, et al. Hippocampal silent infarct leads to subtle cognitive decline that is associated with inflammation and gliosis at twenty-four hours after injury in a rat model[J]. Behav Brain Res, 2021,401:113089.
[11] VEDEL A G, HOLMGAARD F, SIERSMA V, et al. Domainspecific cognitive dysfunction after cardiac surgery. a secondary analysis of a randomized trial[J]. Acta Anaesthesiol Scand, 2019,63(6):730-738.
[12] MENG S X, WANG B, LI W T. LncRNA MALAT1 improves cerebral ischemia-reperfusion injury and cognitive dysfunction by regulating miR-142-3p/SIRT1 axis[J]. Int J Neurosci, 2023,133(7):740-753.
[13] FAGIANI F, LANNI C, RACCHI M, et al.(Dys)regulation of synaptic activity and neurotransmitter release by β-amyloid:a look beyond Alzheimer's disease pathogenesis[J]. Front Mol Neurosci, 2021,14:635880.
[14] HAMPEL H, HU Y, HARDY J, et al. The amyloid-β pathway in Alzheimer's disease:a plain language summary[J]. Neurodegener Dis Manag, 2023,13(3):141-149.
[15] HAMPEL H, HARDY J, BLENNOW K, et al. The amyloid-βpathway in Alzheimer's disease[J]. Mol Psychiatry, 2021,26(10):5481-5503.
[16] ALAWODE D O T, FOX N C, ZETTERBERG H, et al. Alzheimer's disease biomarkers revisited from the amyloid cascade hypothesis standpoint[J]. Front Neurosci, 2022,16:837390.
[17] KOCKI J, U?AMEK-KOZIOT M, BOGUCKA-KOCKA A, et al.Dysregulation of amyloid-β protein precursor, β-secretase,presenilin I and 2 genes in the rat selectively vulnerable CAl subfield of hippocampus following transient global brain ischemia[J]. J Alzheimers Dis, 2015,47(4):1047-1056.
[18] BAI S, MAO M H, TIAN L B, et al. Calcium sensing receptor mediated the excessive generation of β-amyloid peptide induced by hypoxia in vivo and in vitro[J]. Biochem Biophys Res Commun, 2015,459(4):568-573.
[19] KAPSA A, SCHNEIDER J A, YU L, et al. Association of stroke and cerebrovascular pathologies with scam susceptibility in older adults[J]. JAMA Neurol, 2023,80(1):49-57.
[20] FETTES P, SCHULZE L, DOWNAR J. Cortico-striatal-thalamic loop circuits of the orbitofrontal cortex:promising therapeutic targets in psychiatric illness[J]. Front Syst Neurosci, 2017(11):25.
[21] JONES D T, GRAFF-RADFORD J. Executive dysfunction and the prefrontal cortex[J]. Continuum(Minneap Minn), 2021,27(6):1586-1601.
[22] YAN Z, REIN B. Mechanisms of synaptic transmission dysregulation in the prefrontal cortex:pathophysiological implications[J]. Mol Psychiatry, 2022,27(1):445-465.
[23] SZCZEPANSKI S M, KNIGHT R T. Insights into human behavior from lesions to the prefrontal cortex[J]. Neuron, 2014,83(5):1002-1018.
基本信息:
中图分类号:R743.3
引用信息:
[1]赵远琴,何燕青,林静,等.脑梗死后认知功能障碍患者血清γ分泌酶水平变化及梗死部位观察[J].山东医药,2025,65(07):20-23.
基金信息:
贵州省卫生健康委科学技术基金项目(gzwkj2021-012)