Abstract

Abstract Overview

Electronically generated electromagnetic fields (EMFs), including common devices like cell phones, Wi-Fi, and smart meters, can produce intense electric and magnetic forces. These forces impact the voltage sensor of voltage-gated calcium channels, leading to increased intracellular calcium [Ca²⁺]i levels.

Connection to Alzheimer's Disease

The calcium hypothesis of Alzheimer's disease (AD) suggests that excessive [Ca²⁺]i contributes to the disease's progression. Through pathways like excessive calcium signaling and the peroxynitrite/oxidative stress/inflammation pathway, elevated [Ca²⁺]i is implicated in the disease progression, amplified by EMFs. This creates a harmful cycle with amyloid-beta protein (Aβ) in AD patients.

Epidemiological and Experimental Evidence

• Epidemiology indicates a link between EMF exposure and early onset AD.
• Animal model studies corroborate that low intensity EMFs lead to neurodegeneration akin to AD, with key molecular markers like Aβ, amyloid precursor protein, and BACE1 being elevated.
• Daily exposure to pulsed EMFs results in universal or near universal onset of neurodegeneration, including AD in rats, which is superficially analogous to digital dementia observed in humans.

Therapeutic Insights

Interestingly, modest increases in [Ca²⁺]i from EMFs can occasionally yield protective, therapeutic effects. These effects, however, are counterbalanced by pathways leading to cellular damage, highlighting a complex interplay between potentially beneficial and harmful impacts of EMFs.

Conclusion

The synthesis of 18 distinct types of evidence demonstrates a compelling case for EMF involvement in the development of Alzheimer's disease. There is a significant concern that advanced, highly pulsed wireless communications could lead to a rise in very early onset AD in the broader population.