切换至 "中华医学电子期刊资源库"

中华脑科疾病与康复杂志(电子版) ›› 2023, Vol. 13 ›› Issue (05) : 315 -319. doi: 10.3877/cma.j.issn.2095-123X.2023.05.010

综述

帕金森病在病理生理学中的研究进展
金刚, 李英真, 施维, 李博()   
  1. 274400 山东菏泽,曹县人民医院神经内科
    250000 济南,解放军联勤保障部队第九六〇医院神经外科
  • 收稿日期:2022-07-28 出版日期:2023-10-15
  • 通信作者: 李博

Research progress of Parkinson's disease in pathophysiology

Gang Jin, Yingzhen Li, Wei Shi, Bo Li()   

  1. Department of Neurology, Caoxian People's Hospital, Heze 274400, China
    Department of Neurosurgery, the 960th Hospital of PLA, Ji'nan 250000, China
  • Received:2022-07-28 Published:2023-10-15
  • Corresponding author: Bo Li
  • Supported by:
    National Natural Science Foundation of China(81471214)
引用本文:

金刚, 李英真, 施维, 李博. 帕金森病在病理生理学中的研究进展[J/OL]. 中华脑科疾病与康复杂志(电子版), 2023, 13(05): 315-319.

Gang Jin, Yingzhen Li, Wei Shi, Bo Li. Research progress of Parkinson's disease in pathophysiology[J/OL]. Chinese Journal of Brain Diseases and Rehabilitation(Electronic Edition), 2023, 13(05): 315-319.

帕金森病(PD)是一种复杂且与年龄相关的神经退行性疾病,其发病机制仍不完全明确。PD的发生和发展与基因遗传、基因突变、线粒体功能障碍、氧化应激反应、免疫炎性机制、胃肠相关功能障碍、神经黑色素过度累积、铁死亡调控机制等密切相关,各因素既能交叉相互促进又能独立发挥作用。本文围绕PD在病理生理学中的发病机制的研究进展展开综述,旨在为PD的治疗及药物开发寻求新思路。

Parkinson's disease (PD) is a complex and age-related neurodegenerative disease, and its pathogenesis is still not fully understood. The occurrence and development of PD are closely related to genetic inheritance, gene mutations, mitochondrial dysfunction, oxidative stress, immune inflammatory mechanisms, gastrointestinal-related dysfunction, excessive accumulation of neuromelanin, and iron death regulation mechanisms. Various factors can cross each other and play an independent role. This paper reviews the research progress on the pathogenesis of PD in pathophysiology, aiming to seek new ideas for the treatment and drug development of PD.

[1]
武雅静,张丽芳,邓远飞.帕金森病患者认知功能的临床分析[J].中华脑科疾病与康复杂志(电子版), 2019, 9(5): 271-276. DOI: 10.3877/cma.j.issn.2095-123X.2019.05.004.
[2]
张文彦,陈韦陶.帕金森病患者人格特征的研究进展[J].中风与神经疾病杂志, 2020, 37(12): 1144-1146. DOI: 10.19845/j.cnki.zfysjjbzz.2020.0543.
[3]
魏颖鸿.帕金森病基因多态性的研究进展[J].实用老年医学, 2019, 33(7): 637-641. DOI: 10.3969/j.issn.1003-9198.2019.07.004.
[4]
Trudler D, Nash Y, Frenkel D. New insights on Parkinson's disease genes: the link between mitochondria impairment and neuroinflammation[J]. J Neural Transm (Vienna), 2015, 122(10): 1409-1419. DOI: 10.1007/s00702-015-1399-z.
[5]
Singh A, Zhi L, Zhang H. LRRK2 and mitochondria: Recent advances and current views[J]. Brain Res, 2019, 1702: 96-104. DOI: 10.1016/j.brainres.2018.06.010.
[6]
刘越存.分子伴侣辅因子CHIP与帕金森病PINK1基因的相互作用研究[D].广州:南方医科大学, 2009. DOI: 10.7666/d.y1553797.
[7]
Linnertz C, Lutz MW, Ervin JF, et al. The genetic contributions of SNCA and LRRK2 genes to Lewy Body pathology in Alzheimer's disease[J]. Hum Mol Genet, 2014, 23(18): 4814-4821. DOI: 10.1093/hmg/ddu196.
[8]
王莉,娄桂予,卞莎莎,等.一例青少年型帕金森病患者Parkin基因的突变鉴定[J].中华医学遗传学杂志, 2019, 36(4): 344-347. DOI: 10.3760/cma.j.issn.1003-9406.2019.04.013.
[9]
Yuan X, Cao B, Wu Y, et al. Association analysis of SNP rs11868035 in SREBF1 with sporadic Parkinson's disease, sporadic amyotrophic lateral sclerosis and multiple system atrophy in a Chinese population[J]. Neurosci Lett, 2018, 664: 128-132. DOI: 10.1016/j.neulet.2017.11.015.
[10]
Giri S, Naiya T, Roy S, et al. A compound heterozygote for GCH1 mutation represents a case of atypical dopa-responsive dystonia[J]. J Mol Neurosci, 2019, 68(2): 214-220. DOI: 10.1007/s12031-019-01301-3.
[11]
Schreglmann SR, Houlden H. VPS13C-another hint at mitochondrial dysfunction in familial Parkinson's disease[J]. Mov Disord, 2016, 31(9): 1340. DOI: 10.1002/mds.26682.
[12]
许琴,罗晓光,初巧红,等.中国北方女性帕金森病患者与线粒体ND4基因A11084G位点的相关性研究[J].中华神经医学杂志, 2017, 16(4): 392-397. DOI: 10.3760/cma.j.issn.1671-8925.2017.04.013.
[13]
汪志鹏,高歌,段春礼,等. α-突触核蛋白对线粒体膜造成孔道样损伤[J].中国生物化学与分子生物学报, 2018, 34(9): 1013-1020. DOI: 10.13865/j.cnki.cjbmb.2018.09.14.
[14]
Mortiboys H, Johansen KK, Aasly JO, et al. Mitochondrial impairment in patients with Parkinson disease with the G2019S mutation in LRRK2[J]. Neurology, 2010, 75(22): 2017-2020. DOI: 10.1212/WNL.0b013e3181ff9685.
[15]
Hu ZL, Sun T, Lu M, et al. Kir6.1/K-ATP channel on astrocytes protects against dopaminergic neurodegeneration in the MPTP mouse model of Parkinson's disease via promoting mitophagy[J]. Brain Behav Immun, 2019, 81: 509-522. DOI: 10.1016/j.bbi.2019.07.009.
[16]
Rango M, Bresolin N. Brain mitochondria, aging, and Parkinson's disease[J]. Genes (Basel). 2018, 9(5): 250. DOI: 10.3390/genes9050250.
[17]
Bury AG, Pyle A, Elson JL, et al. Mitochondrial DNA changes in pedunculopontine cholinergic neurons in Parkinson disease[J]. Ann Neurol, 2017, 82(6): 1016-1021. DOI: 10.1002/ana.25099.
[18]
Azkona G, López de Maturana R, et al. LRRK2 Expression is deregulated in fibroblasts and neurons from Parkinson patients with mutations in PINK1LRRK2 expression is deregulated in fibroblasts and neurons from Parkinson patients with mutations in PINK1[J]. Mol Neurobiol, 2018, 55(1): 506-516. DOI: 10.1007/s12035-016-0303-7.
[19]
Puspita L, Chung SY, Shim JW. Oxidative stress and cellular pathologies in Parkinson's disease[J]. Mol Brain, 2017, 10(1): 53. DOI: 10.1186/s13041-017-0340-9.
[20]
von Leden RE, Yauger YJ, Khayrullina G, et al. Central nervous system injury and nicotinamide adenine dinucleotide phosphate oxidase: oxidative stress and therapeutic targets[J]. J Neurotrauma, 2017, 34(4): 755-764. DOI: 10.1089/neu.2016.4486.
[21]
Steiner RE, Ibba M. Bridging the gap between tRNA modifications and the respiratory chain[J]. Biochemistry, 2018, 57(18): 2565-2566. DOI: 10.1021/acs.biochem.8b00377.
[22]
Krashia P, Martini A, Nobili A, et al. On the properties of identified dopaminergic neurons in the mouse substantia nigra and ventral tegmental area[J]. Eur J Neurosci, 2017, 45(1): 92-105. DOI: 10.1111/ejn.13364.
[23]
Milovanovi B, Ili J, Stankovi IM, et al. A simulation of free radicals induced oxidation of dopamine in aqueous solution[J]. Chemical Physics, 2019, 524: 26-30. DOI: 10.1016/j.chemphys.2019.05.001.
[24]
Kim A, Kozina E, Kolacheva A, et al. Cooperative synthesis of dopamine by striatal non-dopaminergic neurons as a mechanism of neuroplasticity at parkinsonism[J]. Parkinsonism & Related Disorders, 2018, 46(2): e26-e27. DOI: 10.1016/j.parkreldis.2017.11.086.
[25]
Weng M, Xie X, Liu C, et al. The sources of reactive oxygen species and its possible role in the pathogenesis of Parkinson's disease[J]. Parkinsons Dis, 2018, 2018: 9163040. DOI: 10.1155/2018/9163040.
[26]
Seaton TA, Cooper JM, Schapira AH. Free radical scavengers protect dopaminergic cell lines from apoptosis induced by complex I inhibitors[J]. Brain Res, 1997, 777(1-2): 110-8. DOI: 10.1016/s0006-8993(97)01034-2.
[27]
Faucheux BA, Martin ME, Beaumont C, et al. Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease[J]. J Neurochem, 2019, 86(5): 1142-1148. DOI: 10.1046/j.1471-4159.2003.01923.x.
[28]
Dexter DT, Carter CJ, Wells FR, et al. Basal lipid peroxidation in substantia nigra is increased in Parkinson's disease[J]. J Neurochem, 2010, 52(2): 381-389. DOI: 10.1111/j.1471-4159.1989.tb09133.x.
[29]
Jenner P, Dexter DT, Sian J, et al. Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. The Royal kings and queens Parkinson's disease research group[J]. Ann Neurol, 1992, 32: S82-S87. DOI: 10.1002/ana.410320714.
[30]
Mogi M, Harada M, Kondo T, et al. Transforming growth factor-beta 1 levels are elevated in the striatum and in ventricular cerebrospinal fluid in Parkinson's disease[J]. Neurosci Lett, 1995, 193(2): 129-132. DOI: 10.1016/0304-3940(95)11686-q.
[31]
De Astis S, Corradini I, Morini R, et al. Nanostructured TiO2 surfaces promote polarized activation of microglia, but not astrocytes, toward a proinflammatory profile[J]. Nanoscale, 2013, 5(22): 10963-10974. DOI: 10.1039/c3nr03534d.
[32]
Stypuła G, Kunert-Radek J, Stepień H, et al. Evaluation of interleukins, ACTH, cortisol and prolactin concentrations in the blood of patients with Parkinson's disease[J]. Neuroimmunomodulation, 1996, 3(2-3): 131-134. DOI: 10.1159/000097237.
[33]
Sommer A, Marxreiter F, Krach F, et al. Th17 lymphocytes induce neuronal cell death in a human iPSC-based model of Parkinson's disease[J]. Cell Stem Cell, 2018, 23(1): 123-131.e6. DOI: 10.1016/j.stem.2018.06.015.
[34]
Uemura N, Yagi H, Uemura MT, et al. Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve[J]. Mol Neurodegener, 2018, 13(1): 21. DOI: 10.1186/s13024-018-0257-5.
[35]
Pape HC, Dwenger A, Remmers D, et al. 45 Pattern of intestinal permeability changes and inflammatory response in polytrauma patients[J]. Shock, 1995, 3(5): 14.
[36]
Plascencia Germán, Perry G. Implication of ferroptosis iron-dependent programmed cell death mechanism in neurodegeneration: molecular and cell biology/oxidative stress[J]. Alzheimer's & Dementia, 2020, 16(s3): 1-2. DOI: 10.1002/alz.043978.
[37]
Umemura M, Kim JH, Aoyama H, et al. The iron chelating agent, deferoxamine detoxifies Fe(Salen)-induced cytotoxicity[J]. J Pharmacol Sci, 2017, 134(4): 203-210. DOI: 10.1016/j.jphs.2017.07.002.
[38]
姜宏,陈文芳,谢俊霞.帕金森病模型大鼠脑内多巴胺与铁含量的关系[J].生理学报, 2001, 53(5): 329-333. DOI: 10.3321/j.issn:0371-0874.2001.05.002.
[39]
Faucheux BA, Martin ME, Beaumont C, et al. Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease[J]. J Neurochem, 2010, 86(5): 1142-1148. DOI: 10.1046/j.1471-4159.2003.01923.x.
[40]
Vosahlikova M, Ujcikova H, Hlouskova M, et al. Induction of oxidative stress by long-term treatment of live HEK293 cells with therapeutic concentration of lithium is associated with down-regulation of δ-opioid receptor amount and function[J]. Biochem Pharmacol, 2018, 154: 452-463. DOI: 10.1016/j.bcp.2018.06.004.
[1] 刘璐璐, 何羽. 慢性阻塞性肺病患者睡眠障碍的研究进展[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(05): 836-839.
[2] 廖江荣, 吴秀琳, 陈光春, 郭亮, 吕慈, 蔡俊, 陈夕. 急性主动脉夹层并发急性肺损伤的研究新进展[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(03): 488-492.
[3] 陈华萍, 陈晓龙, 胡明冬. 难治性哮喘的发病机制及诊治进展[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(01): 144-147.
[4] 赵静, 张嘉欣, 高言, 谢席胜. 微小病变肾病的发病机制及治疗研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(04): 207-212.
[5] 孙鼎, 王滨, 陈香美, 陈意志. 热应激肾病的研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(03): 170-176.
[6] 许厅, 熊智倩, 刘俪婷, 姜燕, 苏朝江, 刘宗旸. 维持性血液透析患者皮肤瘙痒症的发病机制及治疗研究进展[J/OL]. 中华肾病研究电子杂志, 2023, 12(06): 334-338.
[7] 贾红艳, 王丹, 张冉冉, 马茜, 焦永红. 基于全外显子组测序探寻Möbius综合征发病机制的遗传学研究[J/OL]. 中华眼科医学杂志(电子版), 2024, 14(03): 146-154.
[8] 曾倩, 徐朝阳, 张丽芳. 帕金森病步态分析的研究进展[J/OL]. 中华脑科疾病与康复杂志(电子版), 2024, 14(04): 235-238.
[9] 安亚楠, 王端然, 郭甜甜, 武希润. 幽门螺杆菌阴性胃黏膜相关淋巴组织淋巴瘤的研究进展[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(03): 268-274.
[10] 刘琦, 王守凯, 王帅, 苏雨晴, 马壮, 陈海军, 司丕蕾. 乳腺癌肿瘤内微生物组的研究进展[J/OL]. 中华临床医师杂志(电子版), 2024, 18(09): 841-845.
[11] 陈雪芬, 韦虹羽, 孙起翔, 赵华, 闫萍, 龚臣. 肺肝样腺癌诊治研究进展[J/OL]. 中华临床医师杂志(电子版), 2024, 18(01): 83-86.
[12] 耿磊, 张照婷, 许磊, 黄海, 孙毅, 杨伏猛, 徐凯, 胡春峰. 帕金森病前驱期基底神经节环路磁共振弥散张量成像的应用研究[J/OL]. 中华临床医师杂志(电子版), 2023, 17(09): 995-1003.
[13] 厉若男, 宋进, 王玉忠. 带状疱疹后神经痛的发病机制和诊治研究进展[J/OL]. 中华诊断学电子杂志, 2024, 12(03): 199-205.
[14] 王可涵, 许涛, 周全红. 围术期谵妄与应激的研究进展[J/OL]. 中华老年病研究电子杂志, 2024, 11(03): 45-49.
[15] 陆远欣, 龚莉琳, 曾梦华. 肥胖与非酒精性脂肪肝研究进展[J/OL]. 中华肥胖与代谢病电子杂志, 2024, 10(02): 113-119.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?