Étude sur l’influence des technologies sans fils à faible intensité et le développement précoce de la maladie d’Alzheimer
Les champs électromagnétiques de faible intensité agissent via l’activation du “canal calcique voltage dépendant” (VGCC) pour provoquer la maladie d’Alzheimer à un stade très précoce : 18 types de preuves distincts – 11 mars 2022 – BETHAM SCIENCE –
Auteur: Martin L.Pall (Professeur émérite de biochimie et de science médicale de base de l’Université de l’État de Washington – USA).
Les champs électromagnétiques (CEM) générés électroniquement, y compris ceux utilisés dans les communications sans fil telles que les téléphones cellulaires, le Wi-Fi et les compteurs intelligents, sont cohérents et produisent des intensités électriques et magnétiques très élevées, qui agissent sur le capteur de tension des canaux calciques dépendant du voltage pour produire des augmentations du calcium intracellulaire [Ca2+]i.
L’hypothèse calcique de la maladie d’Alzheimer (MA) a montré que chacun des éléments causaux importants, spécifiques et non spécifiques de la MA, est produit par un excès de [Ca2+]i. Le [Ca2+]i agit dans la MA par le biais d’une signalisation calcique excessive et de la voie peroxynitrite/stress oxydatif/inflammation, qui sont tous deux élevés par les CEM.Un cercle vicieux apparent dans la MA implique la protéine amyloïde-bêta (Aβ) et le [Ca2+]i.
Trois types d’épidémiologie suggèrent que les CEM sont à l’origine de la MA, y compris de la MA précoce. Des études approfondies sur des modèles animaux montrent que les CEM de faible intensité provoquent une neurodégénérescence, y compris la MA, les animaux atteints de MA présentant des taux élevés d’Aβ, de protéine précurseur d’amyloïde et de BACE1. Les rats exposés quotidiennement à des CEM pulsés développeraient une neurodégénérescence universelle ou quasi universelle à un stade très précoce, y compris la MA ; ces résultats sont superficiellement similaires à ceux des humains atteints de démence digitale. Les CEM produisant des augmentations modestes de [Ca2+]i peuvent également produire des effets thérapeutiques protecteurs. La voie thérapeutique et la voie des peroxynitrites s’inhibent mutuellement.
L’auteur présente un résumé de 18 résultats différents qui, ensemble, fournissent des preuves solides de l’implication des CEM dans la démence. L’auteur craint que les communications sans fil “intelligentes”, plus intelligentes et plus fortement pulsées, ne soient à l’origine de l’apparition généralisée de la MA à un stade très précoce dans les populations humaines.
source: “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” – 11 March 2022. Lien vers le site de Betham Science.
References
[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]