Title:Low Intensity Electromagnetic Fields Act via Voltage-Gated Calcium
Channel (VGCC) Activation to Cause Very Early Onset Alzheimer’s Disease:
18 Distinct Types of Evidence
Volume: 19
Issue: 2
关键词:
阿尔茨海默病钙假说,非热电磁场效应,作为电磁场直接作用对象的电压传感器,阿尔茨海默病动物模型,EMF安全指导衰败、凋亡和自噬细胞的死亡,Aβ和[Ca2+]i恶性循环
摘要: Electronically generated electromagnetic fields (EMFs), including those used in wireless
communication such as cell phones, Wi-Fi and smart meters, are coherent, producing very high electric
and magnetic forces, which act on the voltage sensor of voltage-gated calcium channels to produce increases
in intracellular calcium [Ca2+]i. The calcium hypothesis of Alzheimer’s disease (AD) has shown
that each of the important AD-specific and nonspecific causal elements is produced by excessive
[Ca2+]i. [Ca2+]i acts in AD via excessive calcium signaling and the peroxynitrite/oxidative
stress/inflammation pathway, which are each elevated by EMFs.An apparent vicious cycle in AD involves
amyloid-beta protein (Aβ) and [Ca2+]i. Three types of epidemiology suggest EMF causation of
AD, including early onset AD. Extensive animal model studies show that low intensity EMFs cause neurodegeneration,
including AD, with AD animals having elevated levels of Aβ, amyloid precursor protein
and BACE1. Rats exposed to pulsed EMFs every day are reported to develop universal or near universal
very early onset neurodegeneration, including AD; these findings are superficially similar to humans
with digital dementia. EMFs producing modest increases in [Ca2+]i can also produce protective, therapeutic
effects. The therapeutic pathway and peroxynitrite pathway inhibit each other. A summary of 18
different findings is provided, which collectively provide powerful evidence for EMF causation of AD.
The author is concerned that smarter, more highly pulsed “smart” wireless communication may cause
widespread very, very early onset AD in human populations.