PMID:26972535

Citation	Jiang, DP, Li, JH, Zhang, J, Xu, SL, Kuang, F, Lang, HY, Wang, YF, An, GZ, Li, J and Guo, GZ (2016) Long-term electromagnetic pulse exposure induces Abeta deposition and cognitive dysfunction through oxidative stress and overexpression of APP and BACE1. Brain Res. 1642:10-19
Abstract	A progressively expanded literature has been devoted in the past years to the noxious or beneficial effects of electromagnetic field (EMF) to Alzheimer׳s disease (AD). This study concerns the relationship between electromagnetic pulse (EMP) exposure and the occurrence of AD in rats and the underlying mechanisms, focusing on the role of oxidative stress (OS). 55 healthy male Sprague Dawley (SD) rats were used and received continuous exposure for 8 months. Morris water maze (MWM) test was conducted to test the ability of cognitive and memory. The level of OS was detected by superoxide dismutase (SOD) activity and glutathione (GSH) content. We found that long-term EMP exposure induced cognitive damage in rats. The content of β-amyloid (Aβ) protein in hippocampus was increased after long-term EMP exposure. OS of hippocampal neuron was detected. Western blotting and immunohistochemistry (IHC) assay showed that the content of Aβ protein and its oligomers in EMP-exposed rats were higher than that of sham-exposed rats. The content of Beta Site App Cleaving Enzyme (BACE1) and microtubule-associated protein 1 light chain 3-II (LC3-II) in EMP-exposed rats hippocampus were also higher than that of sham-exposed rats. SOD activity and GSH content in EMP-exposed rats were lower than sham-exposed rats (p<0.05). Several mechanisms were proposed based on EMP exposure-induced OS, including increased amyloid precursor protein (APP) aberrant cleavage. Although further study is needed, the present results suggest that long-term EMP exposure is harmful to cognitive ability in rats and could induce AD-like pathological manifestation.
Links	PubMed Online version:10.1016/j.brainres.2016.02.053
Keywords	Alzheimer Disease/metabolism; Alzheimer Disease/psychology; Amyloid Precursor Protein Secretases/metabolism; Amyloid Precursor Protein Secretases/radiation effects; Amyloid beta-Peptides/metabolism; Amyloid beta-Peptides/radiation effects; Amyloid beta-Protein Precursor/metabolism; Amyloid beta-Protein Precursor/radiation effects; Animals; Aspartic Acid Endopeptidases/metabolism; Aspartic Acid Endopeptidases/radiation effects; Cognition/physiology; Cognition/radiation effects; Disease Models, Animal; Electromagnetic Fields; Hippocampus/metabolism; Hippocampus/radiation effects; Male; Maze Learning/radiation effects; Oxidative Stress/radiation effects; Rats; Rats, Sprague-Dawley
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
RAT:BACE1	involved_in	GO:0009314: response to radiation	ECO:0000270: expression pattern evidence used in manual assertion		P		Seeded From UniProt	complete

References

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