Brain Iron Metabolism and CNS Diseases

被引:88
|
作者
Thirupathi, Anand [1 ]
Chang, Yan-Zhong [1 ]
机构
[1] Hebei Normal Univ, Coll Life Sci, Lab Mol Iron Metab, Key Lab Anim Physiol Biochem & Mol Biol Hebei Pro, 20 Nan Er Huan Eastern Rd, Shijiazhuang 050024, Hebei, Peoples R China
来源
关键词
Iron metabolism; Neurodegenerative diseases; Oxidative stress; Alzheimer's disease; Parkinson's disease; TRANSFERRIN; ABSORPTION; HEPHAESTIN; TRANSPORT; GENE; CERULOPLASMIN; MECHANISMS; EXPRESSION; MEMANTINE; DONEPEZIL;
D O I
10.1007/978-981-13-9589-5_1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Iron is the most abundant trace element in the human body. It is well known that iron is an important component of hemoglobin involved in the transport of oxygen. As a component of various enzymes, it participates in the tricarboxylic acid cycle and oxidative phosphorylation. Iron in the nervous system is also involved in the metabolism of catecholamine neurotransmitters and is involved in the formation of myelin. Therefore, iron metabolism needs to be strictly regulated. Previous studies have shown that iron deficiency in the brain during infants and young children causes mental retardation, such as delayed development of language and body balance, and psychomotor disorders. However, if the iron is excessively deposited in the aged brain, it is closely related to the occurrence of various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Friedreich's ataxia. Therefore, it is important to fully study and understand the mechanism of brain iron metabolism and its regulation. On this basis, exploring the relationship between brain iron regulation and the occurrence of nervous system diseases and discovering new therapeutic targets related to iron metabolism have important significance for breaking through the limitation of prevention and treatment of nervous system diseases. This review discusses the complete research history of iron and its significant role in the pathogenesis of the central nervous system (CNS) diseases.
引用
收藏
页码:1 / 19
页数:19
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