期刊
JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY
卷 30, 期 -, 页码 118-123出版社
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.jtemb.2014.11.009
关键词
Alzheimer's disease; APP(swe)/PS1(Delta E9); Transgenic mouse; Iron load
资金
- National Natural Science Foundation of China [81273983]
- Natural Science Foundation of Hebei Province [C2010001471]
- Science and Technology Research Youth Fund Project of Hebei Colleges and Universities [Q2012036]
- Hebei Food and Drug Administration [PT2014053]
Alzheimer's disease (AD) as a neurodegenerative brain disorder is a devastating pathology leading to disastrous cognitive impairments and dementia, associated with major social and economic costs to society. Iron can catalyze damaging free radical reactions. With age, iron accumulates in brain frontal cortex regions and may contribute to the risk of AD. In this communication, we investigated the age-related brain iron load changes in the frontal cortex of 6- and 12-month-old C57BL/6J (C57) and APP(swe)/PS1(Delta E9) (APP/PS1) double transgenic mouse by using graphite furnace atomic absorption spectrometry (GFAAS) and Penis' reaction. In the present study, we also evaluated the age-related changes of DMT1 and FPN1 by using Western blot and qPCR. We found that compared with 6-month-old APP/PS1 mice and the 12-month-old C57 mice, the 12-month-old APP/PS1 mice had increased iron load in the frontal cortex. The levels of DMT1 were significantly increased and the FPN1 were significantly reduced in the frontal cortex of the 12-month-old APP/PS1 mice than that in the 6-month-old APP/PS1 mice and 12-month-old C57 mice. We conclude that in AD damage occurs in conjunction with iron accumulation, and the brain iron load associated with loss control of the brain iron metabolism related protein DMT1 and FPN1 expressions. (C) 2014 Elsevier GmbH. All rights reserved.
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