Authors

Arendash GW, Sanchez-Ramos J, Mori T, Mamcarz M, Lin X, Runfeldt M, Wang L, Zhang G, Sava V, Tan J, Cao C. Electromagnetic field treatment protects against and reverses cognitive impairment in Alzheimer's disease mice. J Alzheimers Dis. Ahead of print, 2009.

Background
There is little information on long-term effects of electromagnetic fields (EMFs) on brain physiology and function. In particular, no controlled long-term studies of possible effects of radiofrequency EMFs on cognitive function have been conducted to date in humans, mice, or animal models for Alzheimer’s disease (AD).

Objective
The objective was to study effects of long-term (7-9 months) EMF exposure on Alzheimer’s disease like cognitive impairment and neuropathology.

Methods
The study was conducted on transgenic (Tg) mice destined to develop Alzheimer’s-like cognitive impairment, and non-transgenic (NT) mice (n=96 in total). It included: 1) young adult long-term study (918 MHz, 0.25 W/kg EMF exposure for 1-hour twice a day starting at age of 2-2.5 months, behavioral testing 2.5, 4-5 and 6-7 months after initiation of EMF exposure); 2) aged adult long-term study (918 MHz, 0.25 W/kg EMF exposure for 1-hour twice a day starting at the age of 5 months, behavioral testing before and after 2, 5 and 8 months of exposure); 3) aged adult acute study to monitor body and brain temperature during and between EMF exposures in 10-15 month animals. After completion of behavioral testing, the mice were euthanatized and their brains were analyzed for amyloid-β (Aβ) and for antioxidant enzyme levels.

Results
Young adult long-term study: Beneficial cognitive effects of chronic EMF exposure were observed in both Tg and NT mice. EMF exposure had essentially no effect on oxidative markers in the hippocampus of Tg mice, and the changes in oxidative markers in NT mice can be interpreted as a decrease in oxidative stress. No effect of EMF exposure on any oxidative markers was observed in the cerebral cortex tissue of either NT or Tg mice. An increase in levels of soluble Aβ in both hippocampus and frontal cortex was detected in EMF-exposed Tg mice.

Aged adult long-term study:No effect of EMF exposure on cognitive performance of cognitively impaired Tg mice was observed during the initial 5 months of EMF exposure, while NT mice showed improved performance on cognitive testing 5 months after exposure initiation. After 8 months of EMF exposure the cognitive performance of EMF-exposed Tg mice was considerably better. Exposed NT mice continued to show better cognitive performance compared to the control NT mice. Substantially lower hyppocampal and cortical Aβ levels and, at the same time, higher levels of soluble Aβ were observed in exposed Tg mice compared to Tg controls. These results, in the authors’ view, suggest that EMF exposure is able to suppress Aβ aggregation in the brain and/or to disaggregate pre-existing Aβ plaques in Tg mice.
No effects of acute EMF exposure on brain or body temperature was observed in Tg or NT mice in the aged adult acute study, which indicates that long-term EMF exposure was required to produce the increase in body temperature (observed in Tg mice during “On” periods of the Aged Adult Long-Term study).

Interpretation and Conclusions
The results of this study suggest that long-term EMF exposure protects against and/or reverse cognitive impairment and Aβ neuropathology in Alzheimer’s disease Tg mice. Several mechanisms may be involved in producing these effects, in particular, the EMF exposure related decrease in brain Aβ aggregation. The authors conclude that EMF exposure may represent a therapeutic treatment against Alzheimer’s disease and a memory-enhancing approach. At the same time, the authors note that caution should be taken in extrapolating these findings to humans because the animals in these experiments experienced whole body EMF exposure, not the local exposure experienced by humans while using cell phones, and Alzheimer’s disease transgenic mice are only a partial model for Alzheimer’s disease.


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