To study the possible mechanism(s) for electromagnetic field-induced cognitive benefits, brain mitochondrial function was evaluated in aged transgenic mice and non-transgenic littermates following one month of daily electromagnetic field exposure.
The authors have recently reported that long-term exposure to radiofrequency electromagnetic fields not only prevents or reverses cognitive impairment in Alzheimer's transgenic mice, but also improves memory in normal mice (Arendash et al. 2010).
Mice (15 -17 months of age) were divided into the following four groups with a total of three to four mice per group: 1) transgenic mice + exposure, 2) transgenic control group, 3) non-transgenic mice + exposure, 4) non-transgenic control group.
| Exposure | Parameters |
|---|---|
|
Exposure 1:
918 MHz
Modulation type:
pulsed
Exposure duration:
two times 1 h/day for 1 month (early morning and late afternoon)
|
|
mice were divided into four treatment groups: i) trangenic (TG) mice exposed to EMF ii) TG mice sham exposed iii) non-trangenic (NT) mice exposed to EMF iv) NT mice sham exposed
| Frequency | 918 MHz |
|---|---|
| Type | |
| Exposure duration | two times 1 h/day for 1 month (early morning and late afternoon) |
| Modulation type | pulsed |
|---|---|
| Repetition frequency | 217 Hz |
| Additional info |
Gaussian minimal-shift keying (GMSK) used as modulation |
| Exposure source | |
|---|---|
| Distance between exposed object and exposure source | 26 cm |
| Setup | mice placed in individual cages which where arranged radially round the antenna inside a 1.2 m x 1.2 m x 1.2 m Faraday cage |
| Sham exposure | A sham exposure was conducted. |
| Measurand | Value | Type | Method | Mass | Remarks |
|---|---|---|---|---|---|
| electric field strength | 17 V/m | minimum | - | - | - |
| electric field strength | 35 V/m | maximum | - | - | - |
| SAR | 0.25 W/kg | minimum | - | whole body | - |
| SAR | 1.05 W/kg | maximum | - | whole body | - |
In transgenic mice, electromagnetic field exposure enhanced brain mitochondrial function by 50-150%, being greatest in cognitively-important brain areas (e.g. cerebral cortex and hippocampus). Electromagnetic field exposure also increased brain mitochondrial function in normal mice, although the enhancement was not as robust and less widespread compared to that of transgenic mice.
The exposure-induced enhancement of brain mitochondrial function in transgenic mice was accompanied by 5-10 fold increases in soluble amyloid beta protein 1-40 within the same mitochondrial preparations, which is apparently indicative of earlier findings that electromagnetic fields disaggregate toxic amyloid beta protein oligomers in brain tissue (Arendash et al. 2010).
Finally, the irradiation-induced mitochondrial enhancement in both transgenic and normal mice occurred through non-thermal effects because brain temperatures were either stable or decreased during/after electromagnetic field exposure.
These findings collectively suggest that brain mitochondrial enhancement may be a primary mechanism through which electromagnetic field exposure provides cognitive benefit to both transgenic and normal mice. Especially in the context that mitochondrial dysfunction is an early and prominent characteristic of Alzheimer's disease pathogenesis, electromagnetic field treatment could have profound value in the disease's prevention and treatment through intervention at the mitochondrial level.
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