Hepcidin and Iron-associated Neurodegenerative Disorders

doi:10.3969/j.issn.2095-1396.2018.01.003

Abstract

Abstract: The abnormally increased iron in the brain is an initial cause of neuronal death at least in some neurodegenerative. By binding to a unique cellular iron exporter，ferroportin 1 result in its endocytosis and degradation，and inhibit the release of duodenal iron to plasma and inhibit the release of iron from macrophage，then regulat the iron homeostasis of the body. Therefore，hepcidin is a new target for pharmacological intervention in these diseases. Reducing iron to normal level or hampering iron to increase with age in the brain is a promising therapeutic strategy for all iron-associated neurodegenerative disorders. Recent studies demonstrated that increasing hepcidin level in the brain could significantly reduce brain iron contents by regulating the expression of iron transport proteins located in the brain-blood barrier （BBB），neurons and astrocytes. This review mainly discusses the role of hepcidin in the brain and its potential therapeutic role in the disease，providing a new strategy for the prevention and treatment of those diseases.

Key words: brain iron metabolism, neurodegenerative disorders, hepcidin

CLC Number:

R964

MA Juan，ZHANG Fa-li，QIAN Zhong-ming. Hepcidin and Iron-associated Neurodegenerative Disorders[J]. Acta Neuropharmacologica, 2018, 8(1): 16-22.

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