Iron and dopamine: a toxic couple

被引：225
作者：
Hare, Dominic J. [1 ,2 ]
Double, Kay L. [3 ]
机构：
[1] Univ Technol Sydney, Elemental Bioimaging Facil, Broadway, NSW, Australia
[2] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia
[3] Univ Sydney, Sydney Med Sch, Sch Med Sci, Discipline Biomed Sci & Brain & Mind Ctr, Darlington, NSW, Australia
来源：
BRAIN | 2016年 / 139卷
关键词：
Parkinson's disease; cellular mechanisms; oxidative stress; neurodegeneration; alpha-synuclein; HUMAN SUBSTANTIA-NIGRA; GLUTATHIONE-PEROXIDASE; 4; PARKINSONS-DISEASE; ALPHA-SYNUCLEIN; NEURODEGENERATIVE DISEASES; OXIDATIVE STRESS; IN-VIVO; NEUROTOXIN; 6-HYDROXYDOPAMINE; MITOCHONDRIAL DYSFUNCTION; NEURONAL DEGENERATION;
D O I：
10.1093/brain/aww022
中图分类号：
R74 [神经病学与精神病学];
学科分类号：
摘要：
Iron accumulation is a cardinal feature of degenerating regions in the Parkinson's disease brain. As a potent pro-oxidant, redox-active iron may be a key player in upstream mechanisms that precipitate cell death in this disorder. Although an elevation in brain iron levels is a normal feature of ageing, the increase is greater in Parkinson's disease; on the other hand, the effects of the disease are most marked in the nigrostriatal dopaminergic system. In this Update, we explain that neurodegeneration in the affected regions may result from the potent redox couple formed by iron and dopamine itself, and discuss the clinical implications of this molecular trait in this dynamic and rapidly moving area of Parkinson's disease research.
引用
收藏
页码：1026 / 1035
页数：10
相关论文
共 104 条
[1]   The SIRT1 activator resveratrol protects SK-N-BE cells from oxidative stress and against toxicity caused by α-synuclein or amyloid-β (1-42) peptide [J].
Albani, Diego ;
Polito, Letizia ;
Batelli, Sara ;
De Mauro, Stefania ;
Fracasso, Claudia ;
Martelli, Giuliana ;
Colombo, Laura ;
Manzoni, Claudia ;
Salmona, Mario ;
Caccia, Silvio ;
Negro, Alessandro ;
Forloni, Gianluigi .
JOURNAL OF NEUROCHEMISTRY, 2009, 110 (05) :1445-1456
[2]   Oxidative stress in neurodegeneration: cause or consequence? [J].
Andersen, JK .
NATURE MEDICINE, 2004, 10 (07) :S18-S25
[3]   Parkinson's Disease Iron Deposition Caused by Nitric Oxide-Induced Loss of β-Amyloid Precursor Protein [J].
Ayton, Scott ;
Lei, Peng ;
Hare, Dominic J. ;
Duce, James A. ;
George, Jessica L. ;
Adlard, Paul A. ;
McLean, Catriona ;
Rogers, Jack T. ;
Cherny, Robert A. ;
Finkelstein, David I. ;
Bush, Ashley I. .
JOURNAL OF NEUROSCIENCE, 2015, 35 (08) :3591-3597
[4]   Ceruloplasmin dysfunction and therapeutic potential for Parkinson disease [J].
Ayton, Scott ;
Lei, Peng ;
Duce, James A. ;
Wong, Bruce X. W. ;
Sedjahtera, Amelia ;
Adlard, Paul A. ;
Bush, Ashley I. ;
Finkelstein, David I. .
ANNALS OF NEUROLOGY, 2013, 73 (04) :554-559
[5]   Biological metals and metal-targeting compounds in major neurodegenerative diseases [J].
Barnham, Kevin J. ;
Bush, Ashley I. .
CHEMICAL SOCIETY REVIEWS, 2014, 43 (19) :6727-6749
[6]   Parkinson's Disease Gene Therapy: Success by Design Meets Failure by Efficacy [J].
Bartus, Raymond T. ;
Weinberg, Marc S. ;
Samulski, R. Jude .
MOLECULAR THERAPY, 2014, 22 (03) :487-497
[7]   DEGENERATION OF SUBSTANTIA-NIGRA IN CHRONIC PARKINSONS-DISEASE VISUALIZED BY TRANSCRANIAL COLOR-CODED REAL-TIME SONOGRAPHY [J].
BECKER, G ;
SEUFERT, J ;
BOGDAHN, U ;
REICHMANN, H ;
REINERS, K .
NEUROLOGY, 1995, 45 (01) :182-184
[8]   Iron neurochemistry in Alzheimer's disease and Parkinson's disease: targets for therapeutics [J].
Belaidi, Abdel A. ;
Bush, Ashley I. .
JOURNAL OF NEUROCHEMISTRY, 2016, 139 :179-197
[9]   FERRITIN, TRANSFERRIN, AND IRON IN SELECTED REGIONS OF THE ADULT AND AGED RAT-BRAIN [J].
BENKOVIC, SA ;
CONNOR, JR .
JOURNAL OF COMPARATIVE NEUROLOGY, 1993, 338 (01) :97-113
[10]   ROLE OF IRON AND IRON CHELATION IN DOPAMINERGIC-INDUCED NEURODEGENERATION - IMPLICATION FOR PARKINSONS-DISEASE [J].
BENSHACHAR, D ;
ESHEL, G ;
RIEDERER, P ;
YOUDIM, MBH .
ANNALS OF NEUROLOGY, 1992, 32 :S105-S110
12345678910