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.
Keywords: Calcium hypothesis of Alzheimer’s disease, non-thermal electromagnetic field effects, the voltage sensor as the direct target of electromagnetic fields, animal models of Alzheimer’s disease, EMF safety guideline failure, apoptotic and autophagic cell death, Aβ and [Ca2+]i vicious cycle.
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb44401.x] [PMID: 7847692]
[http://dx.doi.org/10.1111/j.1474-9726.2007.00295.x] [PMID: 17465978]
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb44398.x] [PMID: 7847664]
[http://dx.doi.org/10.1515/reveh-2015-0001] [PMID: 25879308]
[http://dx.doi.org/10.1016/j.bbamem.2018.08.017] [PMID: 30409513]
[http://dx.doi.org/10.1016/j.bioelechem.2008.02.003] [PMID: 18407807]
[http://dx.doi.org/10.1016/j.bbr.2012.09.045] [PMID: 23032184]
[http://dx.doi.org/10.1007/s00109-018-1677-y] [PMID: 30088035]
[http://dx.doi.org/10.1093/oxfordjournals.aje.a117669] [PMID: 7677130]
[http://dx.doi.org/10.1097/01.ede.0000142147.49297.9d] [PMID: 15475717]
[http://dx.doi.org/10.1111/j.1749-6632.1975.tb35987.x] [PMID: 163612]
[http://dx.doi.org/10.1371/journal.pone.0035751] [PMID: 22558216]