实用老年医学 ›› 2022, Vol. 36 ›› Issue (1): 95-99.doi: 10.3969/j.issn.1003-9198.2022.01.025
李铭麟, 崔檬, 王佳贺
收稿日期:
2021-10-20
出版日期:
2022-01-20
发布日期:
2022-01-25
通讯作者:
王佳贺,Email:wangjhcmusj@163.com
基金资助:
Received:
2021-10-20
Online:
2022-01-20
Published:
2022-01-25
中图分类号:
李铭麟, 崔檬, 王佳贺. 巨噬细胞与阿尔茨海默病相关性的研究进展[J]. 实用老年医学, 2022, 36(1): 95-99.
[1] Hyman B T, Holtzman D M. Apolipoprotein E levels and Alzheimer risk[J]. Ann Neurol, 2015, 77(2): 204-205. [2] PASSAMONTI L, TSVETANOV K A, JONES P S, et al. Neuroinflammation and functional connectivity in Alzheimer’s disease: interactive influences on cognitive performance[J]. J Neurosci, 2019, 39(36): 7218-7226. [3] MAMMANA S, FAGONE P, CAVALLI E, et al. The role of macrophages in neuroinflammatory and neurodegenerative pathways of Alzheimer’s disease, amyotrophic lateral sclerosis, and multiple sclerosis: pathogenetic cellular effectors and potential therapeutic targets[J]. Int J Mol Sci, 2018, 19(3):831. [4] PRINZ M, PRILLER J, SISODIA S S, et al. Heterogeneity of CNS myeloid cells and their roles in neurodegeneration[J]. Nat Neurosci, 2011, 14(10): 1227-1235. [5] WANG J, GU B J, MASTERS C L, et al. A systemic view of Alzheimer disease-insights from amyloid-β metabolism beyond the brain[J]. Nat Rev Neurol, 2017, 13(10): 612-623. [6] JONES M K, NAIR A, GUPTA M. Mast cells in neurodegenerative disease[J]. Front Cell Neurosci, 2019, 13: 171. [7] JAIRANI P S, ASWATHY P M, KRISHNAN D, et al. Apolipoprotein E polymorphism and oxidative stress in peripheral blood-derived macrophage-mediated amyloid-beta phagocytosis in Alzheimer’s disease patients[J]. Cell Mol Neurobiol, 2019, 39(3): 355-369. [8] LEE J W, LEE I H, IIMURA T, et al. Two macrophages, osteoclasts and microglia: from development to pleiotropy[J]. Bone Res, 2021, 9(1): 11. [9] VAN DER KANT R, GOLDSTEIN L S B, OSSENKOPPELE R. Amyloid-β-independent regulators of tau pathology in Alzheimer disease[J]. Nat Rev Neurosci, 2020, 21(1): 21-35. [10] MORRIS G P, CLARK I A, VISSEL B. Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer’s disease[J]. Acta Neuropathol Commun, 2014, 2: 135. [11] LI F, ETELEEB A, BUCHSER W, et al. Weakly activated core inflammation pathways were identified as a central signaling mechanism contributing to the chronic neurodegeneration in Alzheimer’s disease[J]. BioRxiv, 2021.doi:10.1101/2021.08.30.458295. [12] KINNEY J W, BEMILLER S M, MURTISHAW A S, et al. Inflammation as a central mechanism in Alzheimer’s disease[J]. Alzheimers Dement (NY), 2018, 4: 575-590. [13] SUN X, CHEN W D, WANG Y D. β-Amyloid: the key peptide in the pathogenesis of Alzheimer’s disease[J]. Front Pharmacol, 2015, 6: 221. [14] MUNAWARA U, CATANZARO M, XU W, et al. Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer’s disease[J]. Immun Ageing, 2021, 18(1): 29. [15] RENTSENDORJ A, SHEYN J, FUCHS D T, et al. A novel role for osteopontin in macrophage-mediated amyloid-β clearance in Alzheimer’s models[J]. Brain Behav Immun, 2018, 67: 163-180. [16] PICCIONI G, MANGO D, SAIDI A, et al. Targeting microglia-synapse interactions in Alzheimer’s disease[J]. Int J Mol Sci, 2021, 22(5):2342. [17] MARTINEZ F O, GORDON S. The M1 and M2 paradigm of macrophage activation: time for reassessment[J]. F1000Prime Rep, 2014, 6: 13. [18] KIM S Y, NAIR M G. Macrophages in wound healing: activation and plasticity[J]. Immunol Cell Biol, 2019, 97(3): 258-267. [19] DA MESQUITA S, KIPNIS J. DAMed in (Trem) 2 Steps[J]. Cell, 2017, 169(7): 1172-1174. [20] YUAN P, CONDELLO C, KEENE C D, et al. TREM2 haplodeficiency in mice and humans impairs the microglia barrier function leading to decreased amyloid compaction and severe axonal dystrophy[J]. Neuron, 2016, 90(4): 724-739. [21] NI J, WU Z, MENG J, et al. An impaired intrinsic microglial clock system induces neuroinflammatory alterations in the early stage of amyloid precursor protein knock-in mouse brain[J]. J Neuroinflammation, 2019, 16(1): 173. [22] SINGH-MANOUX A, DUGRAVOT A, BRUNNER E, et al. Interleukin-6 and C-reactive protein as predictors of cognitive decline in late midlife[J]. Neurology, 2014, 83(6): 486-493. [23] FINUCANE O M, SUGRUE J, RUBIO-ARAIZ A, et al. The NLRP3 inflammasome modulates glycolysis by increasing PFKFB3 in an IL-1β-dependent manner in macrophages[J]. Sci Rep, 2019, 9(1): 4034. [24] ISING C, VENEGAS C, ZHANG S, et al. NLRP3 inflammasome activation drives tau pathology[J]. Nature, 2019, 575(7784): 669-673. [25] SEMPLE B D, KOSSMANN T, MORGANTI-KOSSMANN M C. Role of chemokines in CNS health and pathology: a focus on the CCL2/CCR2 and CXCL8/CXCR2 networks[J]. J Cereb Blood Flow Metab, 2010, 30(3): 459-473. [26] SALMINEN A. Hypoperfusion is a potential inducer of immunosuppressive network in Alzheimer’s disease[J]. Neurochem Int, 2021, 142: 104919. [27] SCHLEPCKOW K, MONROE K M, KLEINBERGER G, et al. Enhancing protective microglial activities with a dual function TREM2 antibody to the stalk region[J]. EMBO Mol Med, 2020, 12(4): e11227. [28] PONS V, LÉVESQUE P, PLANTE M M, et al. Conditional genetic deletion of CSF1 receptor in microglia ameliorates the physiopathology of Alzheimer’s disease[J]. Alzheimer’s Res Ther, 2021, 13(1): 8. [29] MRDJEN D, PAVLOVIC A, HARTMANN F J, et al. High-dimensional single-cell mapping of central nervous system immune cells reveals distinct myeloid subsets in health, aging, and disease[J]. Immunity, 2018, 48(2):380-395. [30] WYNN T A, CHAWLA A, POLLARD J W. Macrophage biology in development, homeostasis and disease[J]. Nature, 2013, 496(7446): 445-455. [31] MU X, LI Y, FAN G C. Tissue-resident macrophages in the control of infection and resolution of inflammation[J]. Shock, 2021, 55(1): 14-23. [32] YUNNA C, MENGRU H, LEI W, et al. Macrophage M1/M2 polarization[J]. Eur J Pharmacol, 2020, 877: 173090. [33] GUO H, ZHAO Z, ZHANG R, et al. Monocytes in the peripheral clearance of amyloid-β and Alzheimer’s disease[J]. J Alzheimers Dis, 2019, 68(4): 1391-1400. [34] KOZYREV N, ALBERS S, YANG J, et al. Infiltrating hematogenous macrophages aggregate around β-amyloid plaques in an age-and sex-dependent manner in a mouse model of Alzheimer disease[J]. J Neuropathol Exp Neurol, 2020, 79(11): 1147-1162. [35] KOIZUMI T, KERKHOFS D, MIZUNO T, et al. Vessel-associated immune cells in cerebrovascular diseases: from perivascular macrophages to vessel-associated microglia[J]. Front Neurosci, 2019, 13: 1291. [36] FARACO G, PARK L, ANRATHER J, et al. Brain perivascular macrophages: characterization and functional roles in health and disease[J]. J Mol Med (Berl), 2017, 95(11): 1143-1152. [37] XU L, PAN C L, WU X H, et al. Inhibition of Smad3 in macrophages promotes Aβ efflux from the brain and thereby ameliorates Alzheimer’s pathology[J]. Brain Behav Immun, 2021, 95: 154-167. [38] PIMENOVA A A, HERBINET M, GUPTA I, et al. Alzheimer’s-associated PU.1 expression levels regulate microglial inflammatory response[J]. Neurobiol Dis, 2021, 148: 105217. [39] ZHANG N, CUI Y, LI Y, et al. A novel role of nogo proteins: regulating macrophages in inflammatory disease[J]. Cell Molneurobiol, 2021.doi: 10.1007/S10571-021-01124-0. [40] ZHENG H, JIA L, LIU C C, et al. TREM2 promotes microglial survival by activating wnt/β-catenin pathway[J]. J Neurosci, 2017, 37(7): 1772-1784. |
[1] | 李晓燕, 郁志明. 老年心房颤动合并焦虑状态的研究进展[J]. 实用老年医学, 2024, 38(10): 979-982. |
[2] | 顾崇怀, 项学军, 郑元喜, 乔锐, 林松. 达格列净对接受冠状动脉介入治疗的伴有射血分数降低的心力衰竭合并2型糖尿病老年病人疗效观察[J]. 实用老年医学, 2024, 38(10): 1025-1029. |
[3] | 刘瑾, 黄艳秋, 朱毅, 卓莉莉. 沙库巴曲缬沙坦钠对老年慢性心力衰竭病人的影响[J]. 实用老年医学, 2024, 38(10): 1030-1033. |
[4] | 徐寿勇, 袁勇. 老年病人开展双低剂量CT冠状动脉造影的可行性研究[J]. 实用老年医学, 2024, 38(10): 1054-1058. |
[5] | 刘琳, 邬青, 张静, 毛芳莹, 余璐, 任艺婷, 方婷. 老年心力衰竭病人症状感知现状及影响因素分析[J]. 实用老年医学, 2024, 38(5): 461-437. |
[6] | 刘倩慧, 姚子俊, 何玉立, 徐云凡, 吴军. 老年2型糖尿病合并慢性心力衰竭病人HbA1c水平对心脏结构和功能的影响[J]. 实用老年医学, 2024, 38(5): 491-437. |
[7] | 张丽莉, 李静, 丁林锋, 孙静娴, 蔡静波. 颈动脉粥样硬化斑块对非瓣膜性心房颤动病人缺血性脑卒中事件的预测价值[J]. 实用老年医学, 2024, 38(3): 236-239. |
[8] | 查志敏, 刘欢, 王向明, 李秋爽, 郭妍. 心脏瓣膜钙化对老年冠心病病人预后的影响[J]. 实用老年医学, 2024, 38(3): 245-250. |
[9] | 朱晨晨, 秦海东. 斑块侵蚀在急慢性冠脉综合征发生发展中的作用[J]. 实用老年医学, 2024, 38(3): 308-311. |
[10] | 程清, 徐艳, 陈国飞, 邓心悦. 血清血管紧张素Ⅱ和一氧化氮水平与老年慢性心力衰竭病人认知功能障碍的相关性[J]. 实用老年医学, 2024, 38(2): 132-135. |
[11] | 章颖, 谢玲, 叶佳琦, 羌文慧, 严晓云, 姜英, 张清. 层粘连蛋白与老年急性心肌梗死病人主要不良心血管事件的相关性[J]. 实用老年医学, 2024, 38(2): 149-151. |
[12] | 任丽艳. 老年心力衰竭病人血清胆碱酯酶水平与心室重塑的相关性研究[J]. 实用老年医学, 2023, 37(12): 1238-1241. |
[13] | 刘离香, 刘永铭. 巨噬细胞在心力衰竭中的作用及相关治疗研究进展[J]. 实用老年医学, 2023, 37(12): 1270-1273. |
[14] | 陆昊, 邓慧, 王春, 戴阳, 王芹, 王青. 老年慢性心力衰竭稳定期病人心肺功能、运动耐力特征及NT-proBNP和TNT分析[J]. 实用老年医学, 2023, 37(11): 1138-1142. |
[15] | 杨雪, 甯春, 赵娟, 郝敬波, 杨荣礼. 生长分化因子15和细胞因子对老年冠心病合并衰弱病人的诊断价值[J]. 实用老年医学, 2023, 37(10): 1009-1013. |
阅读次数 | ||||||
全文 |
|
|||||
摘要 |
|
|||||
|