Journal article

Tau-mediated iron export prevents ferroptotic damage after ischemic stroke

QZ Tuo, P Lei, KA Jackman, XL Li, H Xiong, ZY Liuyang, L Roisman, ST Zhang, S Ayton, Q Wang, PJ Crouch, K Ganio, XC Wang, L Pei, PA Adlard, YM Lu, R Cappai, JZ Wang, R Liu, AI Bush

Molecular Psychiatry | NATURE PUBLISHING GROUP | Published : 2017

Abstract

Functional failure of tau contributes to age-dependent, iron-mediated neurotoxicity, and as iron accumulates in ischemic stroke tissue, we hypothesized that tau failure may exaggerate ischemia-reperfusion-related toxicity. Indeed, unilateral, transient middle cerebral artery occlusion (MCAO) suppressed hemispheric tau and increased iron levels in young (3-month-old) mice and rats. Wild-type mice were protected by iron-targeted interventions: ceruloplasmin and amyloid precursor protein ectodomain, as well as ferroptosis inhibitors. At this age, tau-knockout mice did not express elevated brain iron and were protected against hemispheric reperfusion injury following MCAO, indicating that tau su..

View full abstract

Grants

Awarded by Australian Research Council


Funding Acknowledgements

We thank Drs Mian Bi, Lars Ittner and Brian Stevens for technical assistance, and Drs Geoffrey Donnan, David Howells and Craig Rosenfeld for critical review of the manuscript. This work was supported by funds from the Australian Research Council, the National Health and Medical Research Council of Australia (NHMRC), the Cooperative Research Center for Mental Health, Alzheimer's Australia Dementia Research Foundation, National Natural Science Foundation of China (81722016, 81571236, 81271403, 81471304, 91632115) and the Fundamental Research Funds for the Central Universities (2015XJGH013, 2017SCU12042). P Lei is supported by the Recruitment Program of Global Young Experts of China.