title: Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
abstract: OBJECTIVE
  With the developing and widely used electromagnetic field (EMF) technology, more and more studies are focusing on the relationship between EMF and Alzheimer's disease (AD). Electromagnetic pulse (EMP) is one type of widely used EMF. This study aimed to clarify whether EMP exposure could induce cognitive and memory impairment, thus finding a possible relationship between EMP and AD.
  
  
  METHODS
  Forty healthy male Sprague Dawley rats were randomly divided into four groups. Animals, respectively, received 100, 1000, and 10,000 pulses EMP (field strength 50 kV/m, repetition rate 100 Hz) exposure and sham exposure when 2 months old. Monthly Morris water maze (MWM) was used to test the changes of cognitive and memory ability. Superoxide dismutase (SOD) activity and glutathione (GSH) content were used as oxidative stress indexes. Expressions of some types of Alzheimer's disease-related proteins were also detected.
  
  
  RESULTS
  After exposure, EMP exposure caused clear cognitive and memory impairment compared with sham exposure group (p <0.05). Determination of oxidation indexes showed decreased SOD activity and GSH content in exposure groups compared with sham group. Immunohistochemical (IHC) staining showed increased beta amyloid protein (Aβ) in EMP exposure groups compared with sham group. Western blot experiments showed increased expressions of Aβ oligomer and beta amyloid protein precursor (APP) in EMP exposure groups. Increased expression of microtubule-associated protein 1 light chain 3-II (LC3-II) was also found.
  
  
  CONCLUSIONS
  The present results showed that EMP exposure can cause long-term impairment in impaired cognition and memory of rats, resulting in AD-like symptoms. This may be induced by enhancing oxidative stress and is related to autophagy dysfunction.
authors.affiliation: Department of Radiation Medicine, Faculty of Preventive Medicine, Fourth Military Medical University, Xi'an, Shaanxi, China.
authors.forename: Da-peng
authors.initials: DP
authors.lastname: Jiang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.forename: Sheng-long
authors.initials: SL
authors.lastname: Xu
authors.forename: Fang
authors.initials: F
authors.lastname: Kuang
authors.forename: Hai-yang
authors.initials: HY
authors.lastname: Lang
authors.forename: Ya-feng
authors.initials: YF
authors.lastname: Wang
authors.forename: Guang-zhou
authors.initials: GZ
authors.lastname: An
authors.forename: Jin-hui
authors.initials: JH
authors.lastname: Li
authors.forename: Guo-zhen
authors.initials: GZ
authors.lastname: Guo
mesh_terms: D000544:Alzheimer Disease / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000096:biosynthesis / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis* / Q000378:metabolism; D000818:Animals; D001343:Autophagy; D003072:Cognition Disorders / Q000201:enzymology / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D004574:Electromagnetic Fields / Q000009:adverse effects*; D005978:Glutathione / Q000378:metabolism; D008297:Male; D018782:Maze Learning; D008568:Memory; D008569:Memory Disorders / Q000201:enzymology / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D005978:Glutathione; D008869:Microtubule-Associated Proteins; D013482:Superoxide Dismutase; C526109:Anxa3 protein, rat