Age-related changes of brain iron load changes in the frontal cortex in APPswe/PS1ΔE9 transgenic mouse model of Alzheimer's disease

• Published in: Journal of trace elements in medicine and biology 2015-04, Vol.30, p.118-123
• Main Authors: Xian-hui, Dong, Wei-juan, Gao, Tie-mei, Shao, Hong-lin, Xie, Jiang-tao, Bai, Jing-yi, Zhao, Xi-qing, Chai
• Format: Article
• Language: English
• Subjects: Aging - metabolism; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Animals; APPswe/PS1ΔE9; Blotting, Western; Cation Transport Proteins - genetics; Cation Transport Proteins - metabolism; Disease Models, Animal; Frontal Lobe - metabolism; Frontal Lobe - pathology; Humans; Iron - metabolism; Iron load; Male; Mice, Inbred C57BL; Mice, Transgenic; Presenilin-1 - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Staining and Labeling; Transgenic mouse
• ISSN: 0946-672X; 1878-3252
• DOI: 10.1016/j.jtemb.2014.11.009

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 APPswe/PS1ΔE9 (APP/PS1) double transgenic mouse by using graphite furnace atomic absorption spectrometry (GFAAS) and Perls’ 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.