The Relationship Between Electromagnetic Pulse And Rats Alzheimer’s Disease And Its Mechanism

With the extensive application of the electromagnetic waves in military, polytechnic,agriculture, medicine and so on, the intensity of electromagnetic fields (EMF) in the livingenvironment has become increasingly enhanced and the spectrum continue to broaden,which greatly increase the strength of human exposure to the electromagnetic energy, andgenerate serious and complex effects. Electromagnetic pulse (EMP), a pulse-EMF, are shorthigh-voltage pulses with an extremely fast rise time, wide spectrum and high energy. EMPhas a very high peak electric field and a very short cycle of action. So the peak specificabsorption rate (SAR) is quite high, but the average SAR is likely to be small, leading theSAR peak-to-average ratio of much larger than the other types of EMF. Thus its impact onthe health of the organism growing cause for concern.Based on the research of EMF on the biological effects of the brain, in recent years, the research on potential damage of EMF exposure to the central nervous system(CNS) hasbecome a hot issue. In the central nervous system diseases, Alzheimer’s disease (AD) hasbecome a serious health and socio-economic issue facing aging society. According to thelatest epidemiological survey, the current global AD prevalence of approximately2660people, with the accelerated aging of the population, the population increased lifeexpectancy, by2050this number will increase4times.The purpose of this study is to clarify the relationship between the the EMP exposureand onset of AD and its mechanism, focusing on oxidative stress as a bridge in the process.There were two mode of EMP exposure in this study. The first one is a single EMP exposurewith50kV/m field strength at rats age two months. The other one is long-term50kV/m fieldstrength EMP exposure starting at rats age two months.The study found that single or long-term50kV/m field strength the EMP exposure cancause damage of Sprague-Dawley (SD) rats spatial cognition and memory. But the twoexposure generated damage effect at different time. Long-term persistent EMP exposuregenerated effect much earlier than the single exposure. In the Morris water maze (MWM)experiment, for the single EMP exposure treatment groups, the high-dose group rats beganto show significantly increased escape latency (impaired spatial memory)12months afterexposure and the low-dose groups also showed significant differences compared to thesham-exposed group18months after exposure. For the long-term exposure groups, the highdose group showed spatial cognition and memory damage four months after the firstexposure. At eight months after the first exposure, all EMP exposure groups showedsignificant differences compared with sham exposure group. In the Y-maze test, long-termexposure rats also showed spatial discrimination memory capacity injury compared withsham exposure. In elevated plus maze and open field test, long-term exposure rats alsoshowed symptoms of anxiety and depression.AD-related proteins were detected on the basis of behavioral experiments.Immunohistochemistry teat showed that two modes of EMP exposure both increased ratbrain amyloid beta protein (Aβ) expression, with more positive cells and deepened staining.In Western Blot test, hippocampus Aβ oligomers, beta-amyloid precursor protein (APP), beta-sites APP-cleaving protease-1(BACE-1) and the autophagy-related microtubule-associated protein light chain3-II (microtubule-associated protein1light chain3-II, LC3-II) expression were significantly increased in EMP exposed rats compared with shamexposure rats.For some of the oxidative stress indicators, tests found two mode EMP exposure bothdecreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity,increased concentration of malondialdehyde (MDA), and reduced glutathione (GSH)concentration in rats hippocampus.For long-term EMP exposure rats, a decrease in hippocampal neurotransmitter contentand a increase in serum inflammatory factors were also found.In addition, for the long-term exposure rats, at8months after irradiation (rats aged10months), antioxidant (melatonin) intraperitoneal injection was carried out. After melatonintreatment，EMP exposure rats showed decreased escape latency in MWM test. At the sametime, the antioxidant capacity has improved significantly. Increased SOD and GSH-Pxactivity, reduced MDA generation and increased GSH content in the hippocampus werefound. Western blot experiments show decreased expression of BACE1and LC3-II in ratbrain hippocampus.In conclusion, this study shows that single or long-term EMP exposure with fieldstrength of50kV/m could result in damage of SD rats’cognitive and memory capacity, andcause changes in AD-related protein molecule expression in rat brain hippocampus. Thisprocess may be related to the oxidative stress in hippocampus nerve cells.