Radiofrequency Fields, Transthyretin, and Alzheimer's Disease

Abstract

Radiofrequency field (RF) exposure provided cognitive benefits in an animal study. In Alzheimer's disease (AD) mice, exposure reduced brain amyloid-beta (Abeta) deposition through decreased aggregation of Abeta and increase in soluble Abeta levels. Based on our studies on humans on RF from wireless phones, we propose that transthyretin (TTR) might explain the findings. In a cross-sectional study on 313 subjects, we used serum TTR as a marker of cerebrospinal fluid TTR. We found a statistically significantly positive beta coefficient for TTR for time since first use of mobile phones and desktop cordless phones combined (P=0.03). The electromagnetic field parameters were similar for the phone types. In a provocation study on 41 persons exposed for 30 min to an 890-MHz GSM signal with specific absorption rate of 1.0 Watt/kg to the temporal area of the brain, we found statistically significantly increased serum TTR 60 min after exposure. In our cross-sectional study, use of oral snuff also yielded statistically significantly increased serum TTR concentrations and nicotine has been associated with decreased risk for AD and to upregulate the TTR gene in choroid plexus but not in the liver, another source of serum TTR. TTR sequesters Abeta, thereby preventing the formation of Abeta plaques in the brain. Studies have shown that patients with AD have lowered TTR concentrations in the cerebrospinal fluid and have attributed the onset of AD to insufficient sequestering of Abeta by TTR. We propose that TTR might be involved in the findings of RF exposure benefit in AD mice.