Brain Hepcidin Suppresses Major Pathologies in Experimental Parkinsonism
Publication in refereed journal

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摘要Despite intensive research on Parkinson disease (PD) for decades, this common neurodegenerative disease remains incurable. We hypothesize that abnormal iron accumulation is a common thread underlying the emergence of the hallmarks of PD, namely mitochondrial dysfunction and α-synuclein accumulation. We investigated the powerful action of the main iron regulator hepcidin in the brain. In both the rotenone and 6-hydroxydopamine models of PD, overexpression of hepcidin by means of a virus-based strategy prevented dopamine neuronal loss and suppressed major pathologies of Parkinsonism as well as motor deficits. Hepcidin protected rotenone-induced mitochondrial deficits by reducing cellular and mitochondrial iron accumulation. In addition, hepcidin decreased α-synuclein accumulation and promoted clearance of α-synuclein through decreasing iron content that leads to activation of autophagy. Our results not only pinpoint a critical role of iron-overload in the pathogenesis of PD but also demonstrate that targeting brain iron levels through hepcidin is a promising therapeutic direction.
著者Tuo LIANG, Zhong-Ming QIAN, Ming-Dao MU, Wing-Ho YUNG, Ya KE
期刊名稱iScience
出版年份2020
月份7
日期24
卷號23
期次7
出版社Elsevier
文章號碼101284
國際標準期刊號2589-0042
語言英式英語

上次更新時間 2020-14-10 於 00:23