Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats

Arch Med Res. 2013 Apr;44(3):178-84. doi: 10.1016/j.arcmed.2013.03.005. Epub 2013 Mar 19.

Abstract

Background and aims: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / etiology
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides / biosynthesis
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / biosynthesis*
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Autophagy
  • Cognition Disorders / enzymology
  • Cognition Disorders / etiology
  • Cognition Disorders / metabolism
  • Cognition Disorders / physiopathology
  • Electromagnetic Fields / adverse effects*
  • Glutathione / metabolism
  • Male
  • Maze Learning
  • Memory
  • Memory Disorders / enzymology
  • Memory Disorders / etiology
  • Memory Disorders / metabolism
  • Memory Disorders / physiopathology
  • Microtubule-Associated Proteins / metabolism
  • Oxidative Stress
  • Rats
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / metabolism
  • Up-Regulation*

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • LC3 protein, rat
  • Microtubule-Associated Proteins
  • Superoxide Dismutase
  • Glutathione