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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Mini-Review Article

低强度电磁场通过电压门控钙通道（VGCC）激活诱发早期阿尔茨海默病：18种不同类型的证据

卷 19, 期 2, 2022

发表于: 11 March, 2022

页: [119 - 132] 页: 14

弟呕挨: 10.2174/1567205019666220202114510

open access plus

摘要

用电子方法产生的电磁场（EMF），与包括用于手机、Wi-Fi和智能仪表等的无线电的电磁场，是一致的。它会产生很高的电力和磁力，作用于电压门控钙通道的电压传感器上，引起细胞内钙[Ca2+]i的增加。阿尔茨海默病（AD）的钙假说表明每一个重要的AD特异性和非特异性诱发因素都是由于过高的[Ca2+]i引起的。[Ca2+]i通过过高的钙信号和过氧亚硝酸盐/氧化应激/炎症通道作用于AD。这些在EMFs作用下都有所升高。AD的一个明显的恶性循环涉及到β-淀粉样蛋白和[Ca2+]i。三种类型的流行病学都表明了EMF引发了AD，包括早期的AD。大量的动物模型研究表明低强度的EMFs会引起神经退化，包括AD。AD动物有着过高的Aβ、淀粉样前体蛋白和BACE1。据报道，每天暴露于脉冲EMFs中的大鼠成长为普遍或接近普遍的非常早期神经变性，包括AD。这些发现表面上与数字痴呆症患者类似。EMFs能引起[Ca2+]i的适度增加，也能产生保护、治疗的作用。治疗途径和过氧化亚硝酸盐途径相互抑制。对18种不同的发现进行总结，它们共同为EMFs与AD之间的因果关系提供了有力的证明。作者担心更智能、更高脉冲的无线通信可能会在人群中诱发广泛非常、非常早期的AD。

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

« Previous Next »
[1]
Berridge MJ. Calcium hypothesis of Alzheimer’s disease. Pflugers Arch 2010; 459(3): 441-9.
[http://dx.doi.org/10.1007/s00424-009-0736-1] [PMID: 19795132]
[2]
Alzheimer’s Association Calcium Hypothesis Workgroup. Calcium Hypothesis of Alzheimer’s disease and brain aging: A framework for integrating new evidence into a comprehensive theory of pathogenesis. Alzheimers Dement 2017; 13(2): 178-82.
[3]
Bojarski L, Herms J, Kuznicki J. Calcium dysregulation in Alzheimer’s disease. Neurochem Int 2008; 52(4-5): 621-33.
[http://dx.doi.org/10.1016/j.neuint.2007.10.002] [PMID: 18035450]
[4]
Tong BC, Wu AJ, Li M, Cheung KH. Calcium signaling in Alzheimer’s disease & therapies. Biochim Biophys Acta Mol Cell Res 2018; 1865(11 Pt B): 1745-60.
[http://dx.doi.org/10.1016/j.bbamcr.2018.07.018] [PMID: 30059692]
[5]
Celsi F, Pizzo P, Brini M, et al. Mitochondria, calcium and cell death: A deadly triad in neurodegeneration. Biochim Biophys Acta 2009; 1787(5): 335-44.
[http://dx.doi.org/10.1016/j.bbabio.2009.02.021] [PMID: 19268425]
[6]
Wojda U, Salinska E, Kuznicki J. Calcium ions in neuronal degeneration. IUBMB Life 2008; 60(9): 575-90.
[http://dx.doi.org/10.1002/iub.91] [PMID: 18478527]
[7]
Glaser T, Arnaud Sampaio VF, Lameu C, Ulrich H. Calcium signalling: A common target in neurological disorders and neurogenesis. Semin Cell Dev Biol 2019; 95: 25-33.
[http://dx.doi.org/10.1016/j.semcdb.2018.12.002] [PMID: 30529426]
[8]
Mattson MP. Calcium and neuronal injury in Alzheimer’s disease. Contributions of beta-amyloid precursor protein mismetabolism, free radicals, and metabolic compromise. Ann N Y Acad Sci 1994; 747: 50-76.
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb44401.x] [PMID: 7847692]
[9]
Supnet C, Bezprozvanny I. The dysregulation of intracellular calcium in Alzheimer disease. Cell Calcium 2010; 47(2): 183-9.
[http://dx.doi.org/10.1016/j.ceca.2009.12.014] [PMID: 20080301]
[10]
Green KN, LaFerla FM. Linking calcium to Abeta and Alzheimer’s disease. Neuron 2008; 59(2): 190-4.
[http://dx.doi.org/10.1016/j.neuron.2008.07.013] [PMID: 18667147]
[11]
Thibault O, Gant JC, Landfield PW. Expansion of the calcium hypothesis of brain aging and Alzheimer’s disease: minding the store. Aging Cell 2007; 6(3): 307-17.
[http://dx.doi.org/10.1111/j.1474-9726.2007.00295.x] [PMID: 17465978]
[12]
Khachaturian ZS. Calcium hypothesis of Alzheimer’s disease and brain aging. Ann N Y Acad Sci 1994; 747: 1-11.
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb44398.x] [PMID: 7847664]
[13]
The current status of the calcium hypothesis of brain aging and Alzheimer’s disease. Heidelberg, Germany, October 23-25, 1995. Proceedings of a conference. Life Sci 1996; 59(5-6): 357-510.
[14]
O’Day DH, Myre MA. Calmodulin-binding domains in Alzheimer’s disease proteins: extending the calcium hypothesis. Biochem Biophys Res Commun 2004; 320(4): 1051-4.
[http://dx.doi.org/10.1016/j.bbrc.2004.06.070] [PMID: 15249195]
[15]
Popugaeva E, Pchitskaya E, Bezprozvanny I. Dysregulation of neuronal calcium homeostasis in Alzheimer’s disease - A therapeutic opportunity? Biochem Biophys Res Commun 2017; 483(4): 998-1004.
[http://dx.doi.org/10.1016/j.bbrc.2016.09.053] [PMID: 27641664]
[16]
Pall ML. Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects. J Cell Mol Med 2013; 17(8): 958-65.
[http://dx.doi.org/10.1111/jcmm.12088] [PMID: 23802593]
[17]
Pall ML. Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6: microwaves act through voltage-gated calcium channel activation to induce biological impacts at non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic field action. Rev Environ Health 2015; 30(2): 99-116.
[http://dx.doi.org/10.1515/reveh-2015-0001] [PMID: 25879308]
[18]
Pall ML. Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression. J Chem Neuroanat 2016; 75(Pt B): 43-51.
[19]
Pall ML. Wi-Fi is an important threat to human health. Environ Res 2018; 164: 405-16.
[http://dx.doi.org/10.1016/j.envres.2018.01.035] [PMID: 29573716]
[20]
Pall ML. Pall ML. How cancer can be caused by microwave frequency electromagnetic field (EMF) exposures: EMF activation of voltagegated calcium channels (VGCCs) can cause cancer including tumor promotion, tissue invasion and metastasis via 15 mechanisms. In: Markov M, Ed. Mobile Communications and Public Health. Boca Raton, FL: CRC Press 2018; pp. 165-86.
[http://dx.doi.org/10.1201/b22486-7]
[21]
Pall ML. Electromagnetic fields act similarly in plants as in animals. Curr Chem Biol 2016; 10(1): 74-82.
[http://dx.doi.org/10.2174/2212796810666160419160433]
[22]
Pall ML. Millimeter (MM) wave and microwave frequency radiation produce deeply penetrating effects: The biology and the physics. Rev Environ Health 2021. [Epub ahead of print]
[23]
Vieira RT, Caixeta L, Machado S, et al. Epidemiology of early-onset dementia: A review of the literature. Clin Pract Epidemiol Ment Health 2013; 9: 88-95.
[http://dx.doi.org/10.2174/1745017901309010088] [PMID: 23878613]
[24]
Pritchard C, Mayers A, Baldwin D. Changing patterns of neurological mortality in the 10 major developed countries-1979-2010. Public Health 2013; 127(4): 357-68.
[http://dx.doi.org/10.1016/j.puhe.2012.12.018] [PMID: 23601790]
[25]
Pritchard C, Rosenorn-Lanng E. Neurological deaths of American adults (55-74) and the over 75's by sex compared with 20 Western countries 1989-2010: Cause for concern. Surg Neurol Int 2015; 6: 123.
[http://dx.doi.org/10.4103/2152-7806.161420] [PMID: 26290774]
[26]
Pritchard C, Silk A, Hansen L. Are rises in electro-magnetic field in the human environment pollutions, the tipping point for increases in neurological deaths in the western world. Med Hypotheses 2019; 127: 76-83.
[http://dx.doi.org/10.1016/j.mehy.2019.03.018] [PMID: 31088653]
[27]
Hallberg O. A trend model for Alzheimer’s mortality. ADMET 2015; 3: 281-6.
[http://dx.doi.org/10.5599/admet.3.3.201]
[28]
1998 ICNIRP safety guidelines [International Commission on non-ionizing radiation protection}. 1998 ICNIRP Guidelines for limiting exposure to time-varying electric, magnetic, and electromagnetic fields (up to 300 GHz). Health Phys 1998; 74: 494-522.
[29]
Azarov JE, Semenov I, Casciola M, Pakhomov AG. Excitation of murine cardiac myocytes by nanosecond pulsed electric field. J Cardiovasc Electrophysiol 2019; 30(3): 392-401.
[http://dx.doi.org/10.1111/jce.13834] [PMID: 30582656]
[30]
Hristov K, Mangalanathan U, Casciola M, Pakhomova ON, Pakhomov AG. Expression of voltage-gated calcium channels augments cell susceptibility to membrane disruption by nanosecond pulsed electric field. Biochim Biophys Acta Biomembr 2018; 1860(11): 2175-83.
[http://dx.doi.org/10.1016/j.bbamem.2018.08.017] [PMID: 30409513]
[31]
Vernier PT, Sun Y, Chen MT, Gundersen MA, Craviso GL. Nanosecond electric pulse-induced calcium entry into chromaffin cells. Bioelectrochemistry 2008; 73(1): 1-4.
[http://dx.doi.org/10.1016/j.bioelechem.2008.02.003] [PMID: 18407807]
[32]
Craviso GL, Choe S, Chatterjee P, Chatterjee I, Vernier PT. Nanosecond electric pulses: a novel stimulus for triggering Ca2+ influx into chromaffin cells via voltage-gated Ca2+ channels. Cell Mol Neurobiol 2010; 30(8): 1259-65.
[http://dx.doi.org/10.1007/s10571-010-9573-1] [PMID: 21080060]
[33]
Raslear TG, Akyel Y, Bates F, Belt M, Lu ST. Temporal bisection in rats: the effects of high-peak-power pulsed microwave irradiation. Bioelectromagnetics 1993; 14(5): 459-78.
[http://dx.doi.org/10.1002/bem.2250140507] [PMID: 8285916]
[34]
Villela D, Suemoto CK, Pasqualucci CA, Grinberg LT, Rosenberg C. Do Copy Number Changes in CACNA2D2, CACNA2D3, and CACNA1D constitute a predisposing risk factor for Alzheimer’s disease? Front Genet 2016; 7: 107.
[http://dx.doi.org/10.3389/fgene.2016.00107] [PMID: 27379157]
[35]
Novotny M, Klimova B, Valis M. Nitrendipine and dementia: Forgotten positive facts? Front Aging Neurosci 2018; 10: 418.
[http://dx.doi.org/10.3389/fnagi.2018.00418] [PMID: 30618724]
[36]
Anekonda TS, Quinn JF, Harris C, Frahler K, Wadsworth TL, Woltjer RL. L-type voltage-gated calcium channel blockade with isradipine as a therapeutic strategy for Alzheimer’s disease. Neurobiol Dis 2011; 41(1): 62-70.
[http://dx.doi.org/10.1016/j.nbd.2010.08.020] [PMID: 20816785]
[37]
Tan Y, Deng Y, Qing H. Calcium channel blockers and Alzheimer’s disease. Neural Regen Res 2012; 7(2): 137-40.
[PMID: 25767489]
[38]
Gholamipour-Badie H, Naderi N, Khodagholi F, Shaerzadeh F, Motamedi F. L-type calcium channel blockade alleviates molecular and reversal spatial learning and memory alterations induced by entorhinal amyloid pathology in rats. Behav Brain Res 2013; 237: 190-9.
[http://dx.doi.org/10.1016/j.bbr.2012.09.045] [PMID: 23032184]
[39]
Copenhaver PF, Anekonda TS, Musashe D, et al. A translational continuum of model systems for evaluating treatment strategies in Alzheimer’s disease: isradipine as a candidate drug. Dis Model Mech 2011; 4(5): 634-48.
[http://dx.doi.org/10.1242/dmm.006841] [PMID: 21596710]
[40]
Koran ME, Hohman TJ, Thornton-Wells TA. Genetic interactions found between calcium channel genes modulate amyloid load measured by positron emission tomography. Hum Genet 2014; 133(1): 85-93.
[http://dx.doi.org/10.1007/s00439-013-1354-8] [PMID: 24026422]
[41]
Pascual-Caro C, Berrocal M, Lopez-Guerrero AM, et al. STIM1 deficiency is linked to Alzheimer’s disease and triggers cell death in SH-SY5Y cells by upregulation of L-type voltage-operated Ca2+ entry. J Mol Med (Berl) 2018; 96(10): 1061-79.
[http://dx.doi.org/10.1007/s00109-018-1677-y] [PMID: 30088035]
[42]
Jiang Y, Xu B, Chen J, et al. Micro-RNA-137 inhibits tau hyperphosphorylation in Alzheimer’s disease and targets the CACNA1C gene in transgenic mice and human neuroblastoma SH-SY5Y cells. Med Sci Monit 2018; 24: 5635-44.
[http://dx.doi.org/10.12659/MSM.908765] [PMID: 30102687]
[43]
Striessnig J, Pinggera A, Kaur G, Bock G, Tuluc P. L-type Ca2+ channels in heart and brain. Wiley Interdiscip Rev Membr Transp Signal 2014; 3(2): 15-38.
[http://dx.doi.org/10.1002/wmts.102] [PMID: 24683526]
[44]
Sobel E, Davanipour Z, Sulkava R, et al. Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer’s disease. Am J Epidemiol 1995; 142(5): 515-24.
[http://dx.doi.org/10.1093/oxfordjournals.aje.a117669] [PMID: 7677130]
[45]
Sobel E, Dunn M, Davanipour Z, Qian Z, Chui HC. Elevated risk of Alzheimer’s disease among workers with likely electromagnetic field exposure. Neurology 1996; 47(6): 1477-81.
[http://dx.doi.org/10.1212/WNL.47.6.1477] [PMID: 8960730]
[46]
Noonan CW, Reif JS, Yost M, Touchstone J. Occupational exposure to magnetic fields in case-referent studies of neurodegenerative diseases. Scand J Work Environ Health 2002; 28(1): 42-8.
[http://dx.doi.org/10.5271/sjweh.645] [PMID: 11871851]
[47]
Hug K, Röösli M, Rapp R. Magnetic field exposure and neurodegenerative diseases--recent epidemiological studies. Soz Praventivmed 2006; 51(4): 210-20.
[http://dx.doi.org/10.1007/s00038-006-5096-4] [PMID: 17193783]
[48]
García AM, Sisternas A, Hoyos SP. Occupational exposure to extremely low frequency electric and magnetic fields and Alzheimer disease: A meta-analysis. Int J Epidemiol 2008; 37(2): 329-40.
[http://dx.doi.org/10.1093/ije/dym295] [PMID: 18245151]
[49]
Håkansson N, Gustavsson P, Johansen C, Floderus B. Neurodegenerative diseases in welders and other workers exposed to high levels of magnetic fields. Epidemiology 2003; 14(4): 420-6.
[http://dx.doi.org/10.1097/01.EDE.0000078446.76859.c9]
[50]
Huss A, Spoerri A, Egger M, Röösli M. Residence near power lines and mortality from neurodegenerative diseases: Longitudinal study of the Swiss population. Am J Epidemiol 2009; 169(2): 167-75.
[http://dx.doi.org/10.1093/aje/kwn297] [PMID: 18990717]
[51]
Qiu C, Fratiglioni L, Karp A, Winblad B, Bellander T. Occupational exposure to electromagnetic fields and risk of Alzheimer’s disease. Epidemiology 2004; 15(6): 687-94.
[http://dx.doi.org/10.1097/01.ede.0000142147.49297.9d] [PMID: 15475717]
[52]
Stronger evidence for an Alzheimer’s EMF connection. Microwave News XVII 1997. Available from: https://microwavenews.com/news/backissues/j-f97issue.pdf
[53]
Röösli M, Lörtscher M, Egger M, et al. Mortality from neurodegenerative disease and exposure to extremely low-frequency magnetic fields: 31 years of observations on Swiss railway employees. Neuroepidemiology 2007; 28(4): 197-206.
[http://dx.doi.org/10.1159/000108111] [PMID: 17851258]
[54]
Moledina S, Khoja A. Letter to the editor: Digital dementia-is smart technology making us dumb? Ochsner J 2018; 18(1): 12.
[55]
Gajewski RR. Pitfalls of E-education: From multimedia to digital dementia? IEEE Xplore: 07, 2016.
[56]
Dossey L. FOMO, digital dementia, and our dangerous experiment. Explore (NY) 2014; 10(2): 69-73.
[http://dx.doi.org/10.1016/j.explore.2013.12.008] [PMID: 24607071]
[57]
Spitzer M. Digitale Demenz Wie wir uns und unsere Kinder um den Verstand bringen. Munich: Droemer Verlag 2012.
[58]
Ahn J-S, Jun H-J, Kim T-S. Factors affecting smartphone dependency and digital dementia. J Inform Technol Appl Manage 2015; 22(3): 35-54.
[59]
Gołaszewska A, Bik W, Motyl T, Orzechowski A. Bridging the gap between Alzheimer’s disease and Alzheimer’s-like diseases in animals. Int J Mol Sci 2019; 20(7): E1664.
[http://dx.doi.org/10.3390/ijms20071664] [PMID: 30987146]
[60]
Tolgskaya MS, Gordon ZV. Pathological Effects of Radio Waves, Translated from Russian by B Haigh. New York, London: Consultants Bureau 1973.
[http://dx.doi.org/10.1007/978-1-4684-8419-9]
[61]
El-Swefy S, Soliman H, Huessein M. Calcium channel blockade alleviates brain injury induced by long term exposure to an electromagnetic field. J Appl Biomed 2008; 6: 153-63.
[http://dx.doi.org/10.32725/jab.2008.019]
[62]
Jackson JS, Witton J, Johnson JD, et al. Altered synapse stability in the early stages of tauopathy. Cell Rep 2017; 18(13): 3063-8.
[http://dx.doi.org/10.1016/j.celrep.2017.03.013] [PMID: 28355559]
[63]
Orrenius S, Gogvadze V, Zhivotovsky B. Calcium and mitochondria in the regulation of cell death. Biochem Biophys Res Commun 2015; 460(1): 72-81.
[http://dx.doi.org/10.1016/j.bbrc.2015.01.137] [PMID: 25998735]
[64]
Yang M, Wei H. Anesthetic neurotoxicity: Apoptosis and autophagic cell death mediated by calcium dysregulation. Neurotoxicol Teratol 2017; 60: 59-62.
[http://dx.doi.org/10.1016/j.ntt.2016.11.004] [PMID: 27856359]
[65]
Khurana VG, Hardell L, Everaert J, Bortkiewicz A, Carlberg M, Ahonen M. Epidemiological evidence for a health risk from mobile phone base stations. Int J Occup Environ Health 2010; 16(3): 263-7.
[http://dx.doi.org/10.1179/oeh.2010.16.3.263] [PMID: 20662418]
[66]
Levitt BB, Lai H. Biological effects from exposure to electromagnetic radiation emitted by cell tower base stations and other antenna arrays. Environ Rev 2010; 18: 369-95.
[http://dx.doi.org/10.1139/A10-018]
[67]
Subhan F, Khan A, Ahmed S, Malik SN, Bakshah ST, Tahir S. Mobile antennas and its impact on human health. J Med Imaging Health Inform 2018; 8: 1266-73.
[http://dx.doi.org/10.1166/jmihi.2018.2296]
[68]
Dwyer MJ, Leeper DB. A current literature report on the carcinogenic properties of ionizing and nonionizing radiation DHEW Publication. NIOSH 1978; pp. 78-134.
[69]
Sadcikova MN. Clinical manifestations of reactions to microwave irradiation in various occupational groups. In: Czerski P, Ostrowski K, Shore ML, Silverman C, Suess MJ, Waldeskog B, Eds. Biological effects and health hazards of microwave radiation. Warsaw: Polish Medical Publishers 1974; pp. 261-7.
[70]
Baranski S, Edelwejn Z. Experimental morphologic and electroencephalographic studies of microwave effects on the nervous system. Ann N Y Acad Sci 1975; 247: 109-16.
[http://dx.doi.org/10.1111/j.1749-6632.1975.tb35987.x] [PMID: 163612]
[71]
Hecht K. Effects of electromagnetic fields: A review of Russian study results 1960-1996. Umwelt Med Gesel 2001; 1: 222-31.
[72]
Dasdag S, Akdag MZ, Kizil G, Kizil M, Cakir DU, Yokus B. Effect of 900 MHz radio frequency radiation on beta amyloid protein, protein carbonyl, and malondialdehyde in the brain. Electromagn Biol Med 2012; 31(1): 67-74.
[http://dx.doi.org/10.3109/15368378.2011.624654] [PMID: 22268730]
[73]
Dasdag S, Akdag MZ, Erdal ME, et al. Long term and excessive use of 900 MHz radiofrequency radiation alter microRNA expression in brain. Int J Radiat Biol 2015; 91(4): 306-11.
[http://dx.doi.org/10.3109/09553002.2015.997896] [PMID: 25529971]
[74]
Shu B, Zhang X, Du G, Fu Q, Huang L. MicroRNA-107 prevents amyloid-β-induced neurotoxicity and memory impairment in mice. Int J Mol Med 2018; 41(3): 1665-72.
[PMID: 29286086]
[75]
Wang T, Shi F, Jin Y, Jiang W, Shen D, Xiao S. Abnormal changes of brain cortical anatomy and the association with plasma microRNA107 level in amnestic mild cognitive impairment. Front Aging Neurosci 2016; 8: 112.
[http://dx.doi.org/10.3389/fnagi.2016.00112] [PMID: 27242521]
[76]
Ruan J, Liu X, Xiong X, et al. miR 107 promotes the erythroid differentiation of leukemia cells via the downregulation of Cacna2d1. Mol Med Rep 2015; 11(2): 1334-9.
[http://dx.doi.org/10.3892/mmr.2014.2865] [PMID: 25373460]
[77]
Miranda M, Morici JF, Zanoni MB, Bekinschtein P. Brain-derived neurotrophic factor: A key molecule for memory in the healthy and the pathological brain. Front Cell Neurosci 2019; 13: 363.
[http://dx.doi.org/10.3389/fncel.2019.00363] [PMID: 31440144]
[78]
Jiang DP, Li J, Zhang J, et al. Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats. Arch Med Res 2013; 44(3): 178-84.
[http://dx.doi.org/10.1016/j.arcmed.2013.03.005] [PMID: 23523687]
[79]
Jiang DP, Li JH, Zhang J, et al. Long-term electromagnetic pulse exposure induces Abeta deposition and cognitive dysfunction through oxidative stress and overexpression of APP and BACE1. Brain Res 2016; 1642: 10-9.
[http://dx.doi.org/10.1016/j.brainres.2016.02.053] [PMID: 26972535]
[80]
Pilla AA. Nonthermal electromagnetic fields: from first messenger to therapeutic applications. Electromagn Biol Med 2013; 32(2): 123-36.
[http://dx.doi.org/10.3109/15368378.2013.776335] [PMID: 23675615]
[81]
Pall ML. Electromagnetic field activation of voltage-gated calcium channels: Role in therapeutic effects. Electromagn Biol Med 2014; 33(4): 251.
[http://dx.doi.org/10.3109/15368378.2014.906447] [PMID: 24712750]
[82]
Patruno A, Constantini E, Ferrone A, et al. Short ELF-EMF exposures targets SIRT1/Nrf2/HO-1 signalling in THP-1 cells. Inter J Mol Sci 21(19): 7284.
[83]
Arendash GW, Mori T, Dorsey M, Gonzalez R, Tajiri N, Borlongan C. Electromagnetic treatment to old Alzheimer’s mice reverses β-amyloid deposition, modifies cerebral blood flow, and provides selected cognitive benefit. PLoS One 2012; 7(4): e35751.
[http://dx.doi.org/10.1371/journal.pone.0035751] [PMID: 22558216]
[84]
Arendash GW. Review of the evidence that transcranial electromagnetic treatment will be a safe and effective therapeutic against Alzheimer’s disease. J Alzheimers Dis 2016; 53(3): 753-71.
[http://dx.doi.org/10.3233/JAD-160165] [PMID: 27258417]
[85]
Söderqvist F, Hardell L, Carlberg M, Mild KH. Radiofrequency fields, transthyretin, and Alzheimer’s disease. J Alzheimers Dis 2010; 20(2): 599-606.
[http://dx.doi.org/10.3233/JAD-2010-1395] [PMID: 20164553]
[86]
Sivandzade F, Prasad S, Bhalerao A, Cucullo L. NRF2 and NF-қB interplay in cerebrovascular and neurodegenerative disorders: Molecular mechanisms and possible therapeutic approaches. Redox Biol 2019; 21: 101059.
[http://dx.doi.org/10.1016/j.redox.2018.11.017] [PMID: 30576920]
[87]
Pall ML. The NO/ONOO-cycle as the central cause of heart failure. Int J Mol Sci 2013; 14(11): 22274-330.
[http://dx.doi.org/10.3390/ijms141122274] [PMID: 24232452]
[88]
Pall ML. Nitric oxide synthase partial uncoupling as a key switching mechanism for the NO/ONOO- cycle. Med Hypotheses 2007; 69(4): 821-5.
[http://dx.doi.org/10.1016/j.mehy.2007.01.070] [PMID: 17448611]
[89]
Barford PA, Blair JA, Eggar C, Hamon C, Morar C, Whitburn SB. Tetrahydrobiopterin metabolism in the temporal lobe of patients dying with senile dementia of Alzheimer type. J Neurol Neurosurg Psychiatry 1984; 47(7): 736-8.
[http://dx.doi.org/10.1136/jnnp.47.7.736] [PMID: 6747650]
[90]
Fakhri S, Pesce M, Patruno A, et al. Attenuation of Nrf2/Keap1/ARE in Alzheimer’s disease by plant secondary metabolites: A mechanistic review. Molecules 2020; 25(21): 21.
[http://dx.doi.org/10.3390/molecules25214926] [PMID: 33114450]
[91]
Pall ML, Levine S. Nrf2, a master regulator of detoxification and also antioxidant, anti-inflammatory and other cytoprotective mechanisms, is raised by health promoting factors. Sheng Li Xue Bao 2015; 67(1): 1-18.
[PMID: 25672622]
[92]
McGrowder DA, Miller F, Vaz K, et al. Cerebrospinal fluid biomarkers of Alzheimer’s disease: Current evidence and future perspectives. Brain Sci 2021; 11(2): 215.
[http://dx.doi.org/10.3390/brainsci11020215] [PMID: 33578866]

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