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Mol Neurobiol. 2017 May;54(4):3078-3101. doi: 10.1007/s12035-016-9879-1. Epub 2016 Apr 2.

Brain Iron Metabolism Dysfunction in Parkinson's Disease.

Author information

1
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.
2
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.
3
Neurochemistry Laboratory, Division of Psychiatric Neurosciences and Genetics and Aging Research Unit, Massachusetts General Hospital, Boston, MA, 02114, USA.
4
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.

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.

KEYWORDS:

Brain iron metabolism; Iron chelation; Iron regulatory protein; Iron transporters; Parkinson’s disease

PMID:
27039308
DOI:
10.1007/s12035-016-9879-1
[Indexed for MEDLINE]

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