[1]曹媛媛,张磊,高淑英,等.脑脊液β淀粉样蛋白42和NLRP3与麻痹性痴呆患者认知功能障碍、精神行为症状及预后的相关性分析[J].卒中与神经疾病杂志,2023,30(02):188-192.[doi:10.3969/j.issn.1007-0478.2023.02.012]
点击复制

脑脊液β淀粉样蛋白42和NLRP3与麻痹性痴呆患者认知功能障碍、精神行为症状及预后的相关性分析()
分享到:

《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第30卷
期数:
2023年02期
页码:
188-192
栏目:
论著
出版日期:
2023-04-20

文章信息/Info

文章编号:
1007-0478(2023)02-0188-05
作者:
曹媛媛张磊高淑英许东梅
102208 北京市昌平区中西医结合医院北区(分院)(曹媛媛 高淑英); 首都医科大学附属北京地坛医院(张磊 许东梅)
关键词:
β淀粉样蛋白42 核苷酸结合寡聚结构样受体蛋白3 麻痹性痴呆 认知功能障碍 精神行为症状 预后
分类号:
R759.1
DOI:
10.3969/j.issn.1007-0478.2023.02.012
文献标志码:
A
摘要:
目的 分析脑脊液β淀粉样蛋白42(β-amyloid peptide 42,Aβ-42)和核苷酸结合寡聚结构样受体蛋白3(Nucleotide-binding oligomeric structure-like receptor protein 3,NLRP3)与麻痹性痴呆(General paresis of insane,GPI)患者认知功能障碍、精神行为症状及预后的相关性。方法 选取2020年1月-2021年9月本院收治的78例GPI患者为研究对象(研究组),另选取同时期本院收治的58例手术行腰椎麻醉的非神经系统疾病患者为对照组; 检测2组患者脑脊液Aβ-42,NLRP3水平,同时分别采用蒙特利尔认知检查量表(Montreal cognitive assessment,MoCA)、神经精神量表问卷(Neuropsychiatric inventory,NPI)评估2组患者认知功能与精神行为症状; 采用Person相关性分析法分析脑脊液Aβ-42,NLRP3水平与MoCA,NPI评分的相关性。研究组患者均随访6个月,随访截止日期为2022年3月31日; 随访结束后根据患者预后将患者分为预后良好组和预后不良组,比较2组Aβ-42,NLRP3水平及其他相关因素; Logistic回归分析影响GPI患者预后不良的危险因素; 绘制受试者工作特征(Receiver operator characteristic,ROC)曲线分析治疗前脑脊液Aβ-42,NLRP3水平对GPI患者预后不良的预测价值。结果 研究组脑脊液Aβ-42水平低于对照组(P<0.05),NLRP3水平高于对照组(P<0.05); 研究组MoCA评分低于对照组(P<0.05),NPI评分高于对照组(P<0.05)。Person相关性分析法显示,脑脊液Aβ-42水平与MoCA评分呈正相关(r=0.583,P<0.05); 脑脊液Aβ-42水平与NPI评分呈负相关(r=-0.562,P<0.05); 脑脊液NLRP3水平与MoCA评分平呈负相关(r=-0.574,P<0.05); 脑脊液NLRP3水平与NPI评分呈正相关(r=0.557,P<0.05)。预后不良组患者反复多次驱梅治疗占比、脑脊液NLRP3水平、NPI评分高于预后良好组(P<0.05); 预后不良组患者脑脊液Aβ-42水平、MoCA评分低于预后良好组(P<0.05)。Logistic回归分析显示,治疗情况、Aβ-42,NLRP3水平、MoCA,NPI评分均是影响GPI患者预后不良的危险因素(P<0.05)。脑脊液Aβ-42,NLRP3水平单独及联合预测GPI患者预后不良的灵敏度分别为84.12%、85.63%、90.35%,ROC曲线下面积(Area under the curve,AUC)分别为0.743、0.769、0.841,特异度分别为66.72%、63.85%、62.48%。结论 脑脊液Aβ-42与NLRP3水平在GPI患者体内表达异常,与GPI患者认知功能障碍、精神行为症状关系密切,可在一定程度上作为评估GPI患者预后不良的预测指标,且两者联合检测效能更高。

参考文献/References:

[1] Sharma SR, Hussain M, Roy D. General paresis of insane: a forgotten entity[J]. Neurol India, 2020, 68(2): 487-488.
[2] Swain K. “Extraordinarily arduous and fraught with danger”: syphilis, Salvarsan, and general paresis of the insane[J]. Lancet Psychiatry, 2018, 5(9): 702-703.
[3] 王苗苗,张新卿.阿尔茨海默病与麻痹性痴呆临床表现及其共性研究进展[J].中国药理学与毒理学杂志,2019,33(6):450.
[4] Han C, Yang Y, Guan Q, et al. New mechanism of nerve injury in Alzheimer's disease: β-amyloid-induced neuronal pyroptosis[J]. J Cell Mol Med, 2020, 24(14): 8078-8090.
[5] Zhang Y, Zhao Y, Zhang J, et al. Mechanisms of NLRP3 inflammasome activation: its role in the treatment of Alzheimer's disease[J]. Neurochem Res, 2020, 45(11): 2560-2572.
[6] Janier M, Hegyi V, Dupin N, et al. 2014 European guideline on the management of syphilis[J]. Journal of the European Academy of Dermatology and Venereology, 2014, 28(12): 1581-1593.
[7] Zhang M, Zhong X, Shi H, et al. BACE1 and other Alzheimer's-related biomarkers in cerebrospinal fluid and plasma distinguish Alzheimer's disease patients from cognitively-impaired neurosyphilis patients[J]. J Alzheimers Dis, 2020, 77(1): 313-322.
[8] 丁琦超, 陆悦,孙旭,等.伴麻痹性痴呆的神经梅毒患者的临床特征及诊断指标分析[J].中风与神经疾病杂志,2022,39(6):518-522.
[9] Upadhyaya S, Pant SB, Dhungana S, et al. Neuropsychiatric manifestations in General Paralysis of Insane(GPI)[J]. Kathmandu Univ Med J(KUMJ), 2020, 18(70): 207-209.
[10] 陈辛茹,宁玉萍,施海姗,等.麻痹性痴呆和阿尔茨海默病患者的认知和精神行为症状比较[J].中华神经科杂志,2014,47(12):841-846.
[11] Daey OI, Lens CE, Fiolet A, et al. Malaria fever therapy for general paralysis of the insane: a historical cohort study[J]. Eur Neurol, 2017, 78(1/2): 56-62.
[12] Yeung C, Lau K, Au YS, et al. Amyloid, tau and risk of Alzheimer's disease: a Mendelian randomization study[J]. Eur J Epidemiol, 2021, 36(1): 81-88.
[13] Sato Y, Takiguchi M, Tamano H, et al. Extracellular Zn2+-Dependent amyloid-β(1-42)neurotoxicity in Alzheimer's disease pathogenesis[J]. Biol Trace Elem Res, 2021, 199(1): 53-61.
[14] Wang L, Liu S, Xu J, et al. Emodin inhibits aggregation of amyloid-β peptide 1-42 and improves cognitive deficits in Alzheimer's disease transgenic mice[J]. J Neurochem, 2021, 157(6): 1992-2007.
[15] Lewczuk P, ukaszewicz-Zajc M, Mroczko P, et al. Clinical significance of fluid biomarkers in Alzheimer's disease[J]. Pharmacol Rep, 2020, 72(3): 528-542.
[16] Sullivan KJ, Blackshear C, Simino J, et al. Association of midlife plasma amyloid-β levels with cognitive impairment in late Life: the ARIC neurocognitive study[J]. Neurology, 2021, 97(11): e1123-e1131.
[17] Lonnemann N, Hosseini S, Marchetti C, et al. The NLRP3 inflammasome inhibitor OLT1177 rescues cognitive impairment in a mouse model of Alzheimer's disease[J]. Proc Natl Acad Sci USA, 2020, 117(50): 32145-32154.
[18] Van Zeller M, Dias D, Sebastião AM, et al. NLRP3 inflammasome: a starring role in amyloid-β- and Tau-driven pathological events in Alzheimer's disease[J]. J Alzheimers Dis, 2021, 83(3): 939-961.
[19] 师强,郑莹莹,杨增烨.核苷酸结合寡聚化结构域样受体蛋白3炎症小体与阿尔茨海默病患者神经炎症反应,氧化应激的相关性分析[J].国际神经病学神经外科学杂志,2021,48(2):115-119.

备注/Memo

备注/Memo:
基金项目:首都医科大学附属北京地坛医院院内科研基金(编号为DTQH201607)
更新日期/Last Update: 2023-04-20