[1]郭婕 亢恺雯 李华 白呦呦 路小伟李智智 王强.肌萎缩侧索硬化症病理机制及治疗研究进展[J].现代中医药,2021,(06):006-10.[doi:10.13424/j.cnki.mtcm.2021.06.002]
　GUO Jie KANG Kaiwen LI Hua BAI Youyou LU XiaoweiLI Zhizhi WANG Qiang.Research Progress on Pathological Mechanism and Treatment of Amyotrophic Lateral Sclerosis[J].Modern Traditional Chinese Medicine,2021,(06):006-10.[doi:10.13424/j.cnki.mtcm.2021.06.002]
点击复制

肌萎缩侧索硬化症病理机制及治疗研究进展
分享到：

《现代中医药》[ISSN:1006-6977/CN:61-1281/TN]

卷:
期数:
2021年06期
页码:
006-10
栏目:
出版日期:
2023-11-19

文章信息/Info

Title:
Research Progress on Pathological Mechanism and Treatment of Amyotrophic Lateral Sclerosis
文章编号:
1672-0571(2021)06-0006-05
作者:
郭婕1 亢恺雯1 李华2 白呦呦2 路小伟2李智智2 王强2; 3; 4
1.陕西中医药大学第二临床医学院，陕西 咸阳 712046；
2.陕西中医药大学针灸推拿学院， 陕西 咸阳 712046；
3.陕西省针药结合重点实验室，陕西 咸阳 712046；
4.咸阳市神经生物学（针灸）重点实验室，陕西 咸阳 712046
Author(s):
GUO Jie1 KANG Kaiwen1 LI Hua2 BAI Youyou2 LU Xiaowei2LI Zhizhi2 WANG Qiang2; 3; 4
1.The Second Clinical Medical School of Shaanxi University of Traditional Chinese Medicine，Shaanxi Xianyang 712046,China；
2.School of Acupuncture and Massage，Shaanxi University of Traditional Chinese Medicine, Shaanxi Xianyang 712046,China；
3.Shaanxi Key Laboratory of Acupuncture and Medicine，Shaanxi Xianyang 712046, China；
4.Xianyang Key Laboratory of Neurobiology (Acupuncture),Shaanxi Xianyang 712046,China
关键词:
关键词：肌萎缩侧索硬化症; 病理机制; 药物治疗; 针刺治疗; 干细胞移植
Keywords:
Key words:Amyotrophic lateral sclerosis; Pathological mechanism; Medication; Acupuncture treatment; Stem cell transplantation
分类号:
R746.4
DOI:
10.13424/j.cnki.mtcm.2021.06.002
文献标志码:
A
摘要:
摘 要：目的 综述肌萎缩侧索硬化症(amyotrophic lateral sclerosis,ALS)的病理机制及治疗研究进展。方法 检索中国知网、万方、PubMed等数据库，检索字段主要包括ALS、病理机制、药物治疗、针刺治疗等。结果 ALS病理机制复杂多样，彼此之间相互作用。目前治疗ALS药物屈指可数，针刺在治疗ALS领域已取得一定成果。结论 积极探索ALS的病理机制并了解其之间相互作用为发现更多ALS治疗靶点提供理论依据。
Abstract:
Abstract：Objective To review the pathological mechanism and treatment of ALS.Methods The databases of CNKI，Wanfang and PubMed were searched.The search fields mainly included ALS，pathological mechanism，drug treatment，acupuncture treatment，etc.Results The pathological mechanisms of ALS were complex and diverse，and they interacted with each other.At present，there are few drugs to treat ALS，and acupuncture has made some achievements in the field of treating ALS.Conclusion Actively explore the pathological mechanism of ALS and understand its interaction，so as to provide a theoretical basis for finding more therapeutic targets of ALS.

参考文献/References:

［1］van Es MA，Hardiman O，Chio A，et al.Amyotrophic lateral sclerosis[J].Lancet,2017 Nov 4,390(10107):2084-2098.
［2］Talbott EO，Malek AM，Lacomis D.The epidemiology of amyotrophic lateral sclerosis[J].Handbook of clinical neurology，2016，138：225-238.
［3］Zarei S，Cart K，Reiley L，et al．A comprehensive review of amyotrophic lateral sclerosis[J].Surg Neurol Int，2015，6(1)：171．
［4］Steve Vucic.Split elbow sign:more evidence for the importance of cortical dysfunction in ALS[J].Journal of Neurology，Neurosurgery & Psychiatry，2019.
［5］Bae Jong Seok，Menon Parvathi，Mioshi Eneida，et al.Cortical hyperexcitability and the split-hand plus phenomenon：pathophysiological insights in ALS[J].Amyotrophic lateral sclerosis & frontotemporal degeneration，2014，15(3-4)：250-256.
［6］Simon Neil G，Lee Michael，Bae Jong Seok，et al.Dissociated lower limb muscle involvement in amyotrophic lateral sclerosis[J].Journal of Neurology,2015,262(6):1424-1432.
［7］Khalaf R，Martin S，Ellis C，et al.Relative preservation of triceps over biceps strength in upper limb-onset ALS：the ‘split elbow’[J].J Neurol Neurosurg Psychiatry,2019 Jul,90(7):730-733.
［8］Menon Parvathi，Kiernan Matthew C，Vucic Steve.Cortical hyperexcitability precedes lower motor neuron dysfunction in ALS[J].Clinical neurophysiology：official journal of the International Federation of Clinical Neurophysiology，2015，126(4)：803-809.
［9］Nimeshan Geevasinga，Parvathi Menon，P.Hande zdinler，et al.Pathophysiological and diagnostic implications of cortical dysfunction in ALS[J].Nature Reviews Neurology，2016，12(11)：651-661.
［10］Saba L，Viscomi M T，Caioli S，et al.Altered Functionality，Morphology，and Vesicular Glutamate Transporter Expression of Cortical Motor Neurons from a Presymptomatic Mouse Model of Amyotrophic Lateral Sclerosis[J].Cerebral cortex (New York：1991)，2016，26(4)：1512-1528.
［11］Smethurst Phillip，Risse Emmanuel，Tyzack Giulia E，et al.Distinct responses of neurons and astrocytes to TDP-43 proteinopathy in amyotrophic lateral sclerosis[J].Brain：a journal of neurology，2020，143(2)：430-440.
［12］Thomas O.Vogler，Joshua R.Wheeler，Eric D.Nguyen，et al.TDP-43 and RNA form amyloid-like myo-granules in regenerating muscle[J].Nature,2018 Nov,563(7732):508-513.
［13］Ditsworth Dara，Maldonado Marcus，McAlonis-Downes Melissa， et al.Mutant TDP-43 within motor neurons drives disease onset but not progression in amyotrophic lateral sclerosis[J].Acta Neuropathol,2017 Jun;133(6):907-922.
［14］Dyer MS，Reale LA，Lewis KE，et al.Mislocalisation of TDP-43 to the cytoplasm causes cortical hyperexcitability and reduced excitatory neurotransmission in the motor cortex[J].Journal of neurochemistry,2020.
［15］Yu CH，Davidson S，Harapas CR，et al.TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS[J].Cell,2020 Oct 29;183(3):636-649.e18.
［16］Brettschneider J，Toledo JB，Van Deerlin VM，et al.Microglial activation correlates with disease progression and upper motor neuron clinical symptoms in amyotrophic lateral sclerosis[J].PLoS ONE，2017，7(6).
［17］Tondo G，Iaccarino L，Cerami C，et al.11C-PK11195 PET-based molecular study of microglia activation in SOD1 amyotrophic lateral sclerosis[J].Annals of Clinical and Translational Neurology，2020，7(9)：1513-1523.
［18］Pehar M，Harlan BA，Killoy KM，et al.Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis[J].Current Pharmaceutical Design，2017，23(33)：5010-5021.
［19］Killoy KM，Harlan BA，Pehar M，et al.FABP7 upregulation induces a neurotoxic phenotype in astrocytes[J].Glia，2020，68(12).
［20］DAmico E，Factor-Litvak P，Santella RM，et al.Clinical perspective on oxidative stress in sporadic amyotrophic lateral sclerosis[J].Free Radic Biol Med,2013,65:509-527.
［21］Wang Z，Bai Z，Qin X，Cheng Y.Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis：A Systematic Review and Meta-Analysis[J].Oxidative Medicine and Cellular Longevity，2019.
［22］Zorov DB，Juhaszova M，Sollott SJ.Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release[J].Physiol Rev,2014,94(3):909-950.
［23］Xiao Y，Karam C，Yi J，et al.ROS-related mitochondrial dysfunction in skeletal muscle of an ALS mouse model during the disease progression[J].Pharmacological research，2018，138：25-36.
［24］van Es MA,Hardiman O,Chio A,et al.Amyotrophic lateral sclerosis[J].Lancet,2017,390(10107):2084-2098.
［25］Yuji Saitoh,Yuji Takahashi.Riluzole for the treatment of amyotrophic lateral sclerosis[J].Neurodegenerative Disease Management,2020,10（15）:343-355.
［26］Andrews JA，Jackson CE，Heiman-Patterson TD，et al.Real-world evidence of riluzole effectiveness in treating amyotrophic lateral sclerosis[J].Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration，2020，21(7-8)：509-518.
［27］孙颖哲.夹脊电针拮抗ALS-SOD1~(G93A)转基因小鼠腰髓神经元兴奋性毒性的机制研究[D].哈尔滨：黑龙江中医药大学,2016.
［28］Scott A.Drug therapy：On the treatment trail for ALS.Nature.2017 Oct 18;550(7676):S120-S121.doi：10.1038/550S120a.PMID：29045376.Drug therapy：On the treatment trail for ALS[J].Nature，2017，550(7676)：S120-S121.
［29］Trias E，Ibarburu S，Barreto-Núez R，et al.Post-paralysis tyrosine kinase inhibition with masitinib abrogates neuroinflammation and slows disease progression in inherited amyotrophic lateral sclerosis[J].Journal of Neuroinflammation，2016，13(1).
［30］Mora JS，Genge A，Chio A，et al.Masitinib as an add-on therapy to riluzole in patients with amyotrophic lateral sclerosis：a randomized clinical trial[J].Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration，2020，21(1-2)：5-14.
［31］贺韵涵,李晓峰,符涛等.针刺干预对肌萎缩侧索硬化症模型小鼠脑及脊髓中 IBA-1和TNF-α表达的影响[J].陕西中医,2020,41(03):292-296.
［32］苏苏,孙远征,王仕林等.夹脊电针对ALS-SOD1~(G93A)小鼠腰髓中p38 MAPK/NF-κB信号通路的影响研究[J].新疆医科大学学报,2019,42(04):541-546,550.
［33］Rothstein JD.Edaravone：A new drug approved for ALS[J].Cell，2017，171(4)：725.
［34］Ikeda K，Iwasaki Y.Edaravone，a Free Radical Scavenger，Delayed Symptomatic and Pathological Progression of Motor Neuron Disease in the Wobbler Mouse[J].PloS one，2015，10(10)：e0140316.
［35］Ohta Y，Nomura E，Shang J，et al.Enhanced oxidative stress and the treatment by edaravone in mice model of amyotrophic lateral sclerosis[J].Journal of Neuroscience Research，2019，97(5)：607-619.
［36］郭静.夹脊电针对ALS-SOD1~(G93A)转基因小鼠腰髓中COX-2表达影响的实验研究[D].哈尔滨：黑龙江中医药大学,2017.
［37］Ciervo Y，Ning K，Jun X，et al.Advances，challenges and future directions for stem cell therapy in amyotrophic lateral sclerosis[J].Molecular Neurodegeneration，2017，12(1).
［38］Gugliandolo A，Bramanti P，Mazzon E.Mesenchymal Stem Cells：A Potential Therapeutic Approach for Amyotrophic Lateral Sclerosis?[J].Stem cells international，2019，2019：3675627.
［39］Sironi F，Vallarola A，Violatto MB，et al.Multiple intracerebroventricular injections of human umbilical cord mesenchymal stem cells delay motor neurons loss but not disease progression of SOD1G93A mice[J].Stem Cell Research，2017，25：166-178.
［40］Oh KW，Noh MY，Kwon MS，et al.Repeated Intrathecal Mesenchymal Stem Cells for Amyotrophic Lateral Sclerosis[J].Annals of Neurology，2018，84(3)：361-373.

备注/Memo

备注/Memo:
基金项目：国家自然科学基金项目（82074555）；陕西省自然科学基础研究计划（2020JM-594）；陕西中医药大学经脉-脏腑相关研究创新团队（YL-09)
更新日期/Last Update: 2021-11-25