title: Brain Iron Metabolism Dysfunction in Parkinson's Disease.
abstract: Dysfunction of iron metabolism, which includes its uptake, storage, and release, plays a key role in neurodegenerative disorders, including Parkinson's disease (PD), Alzheimer's disease, and Huntington's disease. Understanding how iron accumulates in the substantia nigra (SN) and why it specifically targets dopaminergic (DAergic) neurons is particularly warranted for PD, as this knowledge may provide new therapeutic avenues for a more targeted neurotherapeutic strategy for this disease. In this review, we begin with a brief introduction describing brain iron metabolism and its regulation. We then provide a detailed description of how iron accumulates specifically in the SN and why DAergic neurons are especially vulnerable to iron in PD. Furthermore, we focus on the possible mechanisms involved in iron-induced cell death of DAergic neurons in the SN. Finally, we present evidence in support that iron chelation represents a plausable therapeutic strategy for PD.
authors.affiliation: Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao, 266071, China. hongjiang@qdu.edu.cn.
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.affiliation: Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao, 266071, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Neurochemistry Laboratory, Division of Psychiatric Neurosciences and Genetics and Aging Research Unit, Massachusetts General Hospital, Boston, MA, 02114, USA.
authors.forename: Jack
authors.initials: J
authors.lastname: Rogers
authors.affiliation: Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao, 266071, China. jxiaxie@public.qd.sd.cn.
authors.forename: Junxia
authors.initials: J
authors.lastname: Xie
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D007501:Iron / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D010300:Parkinson Disease / Q000378:metabolism*
chemical_list: D007501:Iron
keywords: Brain iron metabolism; Iron chelation; Iron regulatory protein; Iron transporters; Parkinson’s disease