Advances in the pathogenesis of abnormal copper metabolism disorder in Parkinson's disease
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1.Encephalopathy Center,The First Affiliated Hospital of Henan University of Chinese Medicine;2.The First Clinical College of Medicine,Henan University of Chinese Medicine

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    Abstract:

    Parkinson's disease is a neurodegenerative disease associated with abnormal copper metabolism in the brain,which leads to misfolding and aggregation of α-synuclein-copper complexes, which is an important pathological sign of Parkinson's disease. Copper metabolism refers to the cellular metabolic process involving copper ions, which is closely related to the pathogenesis of α-synuclein aggregation, dopamine metabolism, mitochondrial dysfunction, oxidative stress and iron death in Parkinson's disease. In this review, we describe the molecular metabolic mechanism of copper toxicity by studying the pathological role of copper metabolism in Parkinson's disease,in order to provide evidence and help for further improvement of the mechanism of action and drug development.

    Reference
    [1] Feng Y S, Yang S D, Tan Z X, et al. The benefits and mechanisms of exercise training for Parkinson''s disease[J]. Life Sci, 2020,245:117345.
    [2] Bloem B R, Okun M S, Klein C. Parkinson''s disease[J]. Lancet, 2021,397(10291):2284-2303.
    [3] Cabreira V, Massano J. [Parkinson''s Disease: Clinical Review and Update][J]. Acta Med Port, 2019,32(10):661-670.
    [4] Mollenhauer B, von Arnim C. Toward preventing Parkinson''s disease[J]. Science, 2022,377(6608):818-819.
    [5] Bisaglia M, Bubacco L. Copper Ions and Parkinson''s Disease: Why Is Homeostasis So Relevant?[J]. Biomolecules, 2020,10(2).
    [6] Pezacki A T, Matier C D, Gu X, et al. Oxidation state-specific fluorescent copper sensors reveal oncogene-driven redox? changes that regulate labile copper(II) pools[J]. Proc Natl Acad Sci U S A, 2022,119(43):e2092231177.
    [7] Li Y. Copper homeostasis: Emerging target for cancer treatment[J]. IUBMB Life, 2020,72(9):1900-1908.
    [8] Wittung-Stafshede P. Crossroads between copper ions and amyloid formation in Parkinson''s disease[J]. Essays Biochem, 2022,66(7):977-986.
    [9] Gromadzka G, Tarnacka B, Flaga A, et al. Copper Dyshomeostasis in Neurodegenerative Diseases-Therapeutic Implications[J]. Int J Mol Sci, 2020,21(23).
    [10] Liu C, Zhao Y, Xi H, et al. The Membrane Interaction of Alpha-Synuclein[J]. Front Cell Neurosci, 2021,15:633727.
    [11] Li S, Kerman K. Electrochemical Detection of Interaction between Copper(II) and Peptides Related? to Pathological α-Synuclein Mutants[J]. Anal Chem, 2019,91(6):3818-3826.
    [12] Calvo J S, Mulpuri N V, Dao A, et al. Membrane insertion exacerbates the α-Synuclein-Cu(II) dopamine oxidase activity:? Metallothionein-3 targets and silences all α-synuclein-Cu(II) complexes[J]. Free Radic Biol Med, 2020,158:149-161.
    [13] Li Y, Yang C, Wang S, et al. Copper and iron ions accelerate the prion-like propagation of α-synuclein: A? vicious cycle in Parkinson''s disease[J]. Int J Biol Macromol, 2020,163:562-573.
    [14] Lothian A, Lago L, Mukherjee S, et al. Characterization of the metal status of natively purified alpha-synuclein from? human blood, brain tissue, or recombinant sources using size exclusion ICP-MS? reveals no significant binding of Cu, Fe or Zn[J]. Metallomics, 2019,11(1):128-140.
    [15] Lakard S, Pavel I A, Lakard B. Electrochemical Biosensing of Dopamine Neurotransmitter: A Review[J]. Biosensors (Basel), 2021,11(6).
    [16] Latif S, Jahangeer M, Maknoon R D, et al. Dopamine in Parkinson''s disease[J]. Clin Chim Acta, 2021,522:114-126.
    [17] Post M R, Sulzer D. The chemical tools for imaging dopamine release[J]. Cell Chem Biol, 2021,28(6):748-764.
    [18] Li Y, Xia Y, Yin S, et al. Targeting Microglial α-Synuclein/TLRs/NF-kappaB/NLRP3 Inflammasome Axis in? Parkinson''s Disease[J]. Front Immunol, 2021,12:719807.
    [19] Raj K, Kaur P, Gupta G D, et al. Metals associated neurodegeneration in Parkinson''s disease: Insight to? physiological, pathological mechanisms and management[J]. Neurosci Lett, 2021,753:135873.
    [20] Zhou Q, Zhang Y, Lu L, et al. Copper induces microglia-mediated neuroinflammation through ROS/NF-κB pathway and? mitophagy disorder[J]. Food Chem Toxicol, 2022,168:113369.
    [21] Cruces-Sande A, Rodríguez-Pérez A I, Herbello-Hermelo P, et al. Copper Increases Brain Oxidative Stress and Enhances the Ability of? 6-Hydroxydopamine to Cause Dopaminergic Degeneration in a Rat Model of? Parkinson''s Disease[J]. Mol Neurobiol, 2019,56(4):2845-2854.
    [22] Ng M, Wai T, Simonsen A. Quality control of the mitochondrion[J]. Dev Cell, 2021,56(7):881-905.
    [23] Trist B G, Hare D J, Double K L. Oxidative stress in the aging substantia nigra and the etiology of Parkinson''s? disease[J]. Aging Cell, 2019,18(6):e13031.
    [24] Mezzaroba L, Alfieri D F, Colado S A, et al. The role of zinc, copper, manganese and iron in neurodegenerative diseases[J]. Neurotoxicology, 2019,74:230-241.
    [25] Chen J, Gao X, Zheng C, et al. Low-dose Cu exposure enhanced α-synuclein accumulation associates with? mitochondrial impairments in mice model of Parkinson''s disease[J]. Toxicol Lett, 2023,387:14-27.
    [26] van der Pol A, van Gilst W H, Voors A A, et al. Treating oxidative stress in heart failure: past, present and future[J]. Eur J Heart Fail, 2019,21(4):425-435.
    [27] Percário S, Da S B A, Varela E, et al. Oxidative Stress in Parkinson''s Disease: Potential Benefits of Antioxidant? Supplementation[J]. Oxid Med Cell Longev, 2020,2020:2360872.
    [28] Hemmati-Dinarvand M, Saedi S, Valilo M, et al. Oxidative stress and Parkinson''s disease: conflict of oxidant-antioxidant? systems[J]. Neurosci Lett, 2019,709:134296.
    [29] Pyatha S, Kim H, Lee D, et al. Association between Heavy Metal Exposure and Parkinson''s Disease: A Review of the? Mechanisms Related to Oxidative Stress[J]. Antioxidants (Basel), 2022,11(12).
    [30] Maina M B, Al-Hilaly Y K, Burra G, et al. Oxidative Stress Conditions Result in Trapping of PHF-Core Tau (297-391)? Intermediates[J]. Cells, 2021,10(3).
    [31] Behl T, Madaan P, Sehgal A, et al. Mechanistic Insights Expatiating the Redox-Active-Metal-Mediated Neuronal? Degeneration in Parkinson''s Disease[J]. Int J Mol Sci, 2022,23(2).
    [32] Gonzalez-Alcocer A, Gopar-Cuevas Y, Soto-Dominguez A, et al. Combined chronic copper exposure and aging lead to neurotoxicity in vivo[J]. Neurotoxicology, 2023,95:181-192.
    [33] Jiang X, Stockwell B R, Conrad M. Ferroptosis: mechanisms, biology and role in disease[J]. Nat Rev Mol Cell Biol, 2021,22(4):266-282.
    [34] Tang D, Chen X, Kang R, et al. Ferroptosis: molecular mechanisms and health implications[J]. Cell Res, 2021,31(2):107-125.
    [35] Qiu Y, Cao Y, Cao W, et al. The Application of Ferroptosis in Diseases[J]. Pharmacol Res, 2020,159:104919.
    [36] 江全鑫, 陈素贞, 刘军力. 铜蓝蛋白在脂质代谢稳态调控中作用的研究进展[J]. 上海交通大学学报(医学版), 2024,44(01):124-130.
    [37] Yang M, Wu X, Hu J, et al. COMMD10 inhibits HIF1α/CP loop to enhance ferroptosis and radiosensitivity by? disrupting Cu-Fe balance in hepatocellular carcinoma[J]. J Hepatol, 2022,76(5):1138-1150.
    [38] Tsvetkov P, Coy S, Petrova B, et al. Copper induces cell death by targeting lipoylated TCA cycle proteins[J]. Science, 2022,375(6586):1254-1261.
    [39] Singh N, Kallollimath P, Shah M H, et al. Genetic analysis of ATP7B in 102 south Indian families with Wilson disease[J]. PLoS One, 2019,14(5):e215779.
    [40] Hartwig C, Zlatic S A, Wallin M, et al. Trafficking mechanisms of P-type ATPase copper transporters[J]. Curr Opin Cell Biol, 2019,59:24-33.
    [41] Dusek P, Litwin T, Cz?onkowska A. Neurologic impairment in Wilson disease[J]. Ann Transl Med, 2019,7(Suppl 2):S64.
    [42] Kim M J, Oh S B, Kim J, et al. Association of metals with the risk and clinical characteristics of Parkinson''s? disease[J]. Parkinsonism Relat Disord, 2018,55:117-121.
    [43] Altarelli M, Ben-Hamouda N, Schneider A, et al. Copper Deficiency: Causes, Manifestations, and Treatment[J]. Nutr Clin Pract, 2019,34(4):504-513.
    [44] Cendrowska-Pinkosz M, Ostrowska-Lesko M, Ognik K, et al. Dietary Copper Deficiency Leads to Changes in Gene Expression Indicating an? Increased Demand for NADH in the Prefrontal Cortex of the Rat''s Brain[J]. Int J Mol Sci, 2022,23(12).
    [45] Xu J, Su X, Burley S K, et al. Nuclear SOD1 in Growth Control, Oxidative Stress Response, Amyotrophic Lateral? Sclerosis, and Cancer[J]. Antioxidants (Basel), 2022,11(2).
    [46] Shafiq K, Sanghai N, Guo Y, et al. Implication of post-translationally modified SOD1 in pathological aging[J]. Geroscience, 2021,43(2):507-515.
    [47] Trist B G, Davies K M, Cottam V, et al. Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is? associated with neuronal loss in Parkinson''s disease brain[J]. Acta Neuropathol, 2017,134(1):113-127.
    [48] Kuo M, Beckman J S, Shaw C A. Neuroprotective effect of CuATSM on neurotoxin-induced motor neuron loss in an? ALS mouse model[J]. Neurobiol Dis, 2019,130:104495.
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History
  • Received:April 29,2024
  • Revised:June 11,2024
  • Adopted:September 19,2024
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