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.

IF 1.8 4区 医学 Q3 CLINICAL NEUROLOGY
Martin L Pall
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引用次数: 7

Abstract

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.

Abstract Image

Abstract Image

低强度电磁场通过电压门控钙通道(VGCC)激活导致早发性阿尔茨海默病:18种不同类型的证据
电子产生的电磁场(emf),包括用于无线通信的电磁场,如手机、Wi-Fi和智能电表,是连贯的,产生非常高的电磁力,作用于电压门控钙通道的电压传感器,使细胞内钙[Ca2+]i增加。阿尔茨海默病(AD)的钙假说表明,每种重要的AD特异性和非特异性致病因子都是由过量的[Ca2+]i产生的。[Ca2+]i通过过量的钙信号和过氧亚硝酸盐/氧化应激/炎症途径在AD中起作用,这两个途径都被电磁场升高。AD明显的恶性循环涉及淀粉样蛋白- β (Aβ)和[Ca2+]i。三种流行病学类型提示电磁场引起AD,包括早发性AD。大量的动物模型研究表明,低强度电磁场引起包括AD在内的神经退行性变,AD动物的Aβ、淀粉样蛋白前体蛋白和BACE1水平升高。据报道,每天暴露于脉冲电磁场的大鼠会发生普遍或接近普遍的极早发性神经变性,包括阿尔茨海默病;这些发现表面上与患有数字痴呆的人相似。使[Ca2+]i适度增加的电磁场也能产生保护和治疗作用。治疗途径和过氧亚硝酸盐途径相互抑制。本文总结了18项不同的发现,这些发现共同提供了电磁场引起AD的有力证据。作者担心,更智能、更高脉冲的“智能”无线通信可能会在人群中引起广泛的、非常早发的AD。
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来源期刊
Current Alzheimer research
Current Alzheimer research 医学-神经科学
CiteScore
4.00
自引率
4.80%
发文量
64
审稿时长
4-8 weeks
期刊介绍: Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
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