LinkedIn

 آمار

تعداد نشریات20
تعداد شماره‌ها1,149
تعداد مقالات10,518
تعداد مشاهده مقاله45,416,350
تعداد دریافت فایل اصل مقاله11,292,301
Bevelacqua, J J, Mortazavi, S M J. (1397). Alzheimer ’s Disease: Possible Mechanisms Behind Neurohormesis Induced by Exposure to Low Doses of Ionizing Radiation. سامانه مدیریت نشریات علمی, 8(2), 153-156. doi: 10.31661/jbpe.v8i2.919
J J Bevelacqua; S M J Mortazavi. "Alzheimer ’s Disease: Possible Mechanisms Behind Neurohormesis Induced by Exposure to Low Doses of Ionizing Radiation". سامانه مدیریت نشریات علمی, 8, 2, 1397, 153-156. doi: 10.31661/jbpe.v8i2.919
Bevelacqua, J J, Mortazavi, S M J. (1397). 'Alzheimer ’s Disease: Possible Mechanisms Behind Neurohormesis Induced by Exposure to Low Doses of Ionizing Radiation', سامانه مدیریت نشریات علمی, 8(2), pp. 153-156. doi: 10.31661/jbpe.v8i2.919
Bevelacqua, J J, Mortazavi, S M J. Alzheimer ’s Disease: Possible Mechanisms Behind Neurohormesis Induced by Exposure to Low Doses of Ionizing Radiation. سامانه مدیریت نشریات علمی, 1397; 8(2): 153-156. doi: 10.31661/jbpe.v8i2.919

Alzheimer ’s Disease: Possible Mechanisms Behind Neurohormesis Induced by Exposure to Low Doses of Ionizing Radiation

Journal of Biomedical Physics and Engineering
مقاله 1، دوره 8، شماره 2، شهریور 2018، صفحه 153-156    اصل مقاله (383.21 K)
نوع مقاله: Short Communication
شناسه دیجیتال (DOI): 10.31661/jbpe.v8i2.919
نویسندگان
J J Bevelacqua1؛ S M J Mortazavi* 2، 3
1Bevelacqua Resources, 343 Adair Drive, Richland, WA 99352, USA
2Biophotonics Lab, Department of Electrical Engineering, University of Wisconsin Milwaukee, 3200 N Cramer St., Milwaukee, WI 53211, USA
3Ionizing and Non-ionizing Radiation Protection Research Center (INIRPRC), Shiraz University of Medical Sciences, Shiraz, Iran
چکیده
In 2016, scientists reported that human exposure to low doses of ionizing radiation (CT scans of the brain) might relieve symptoms of both Alzheimer’s disease (AD) and Parkinson disease (PD). The findings were unbelievable for those who were not familiar with neurohormesis. X-ray stimulation of the patient’s adaptive protection systems against neurodegenerative diseases was the mechanism proposed by those authors. Now, some more recent studies performed in the field of neurobiological research confirm that low levels of stress can produce protective responses against the pathogenic processes. This paper outlines possible protective consequences of LDR in preventing the pathogenesis of AD through mechanisms such as restoring the myelin sheath and preventing neurodegeneration caused by oxidative stress. Focal demyelination is frequently reported in the proximity of beta-amyloid plaques within neocortex. Extracellular accumulation of amyloid is among well-characterized pathological changes in AD. It should be noted that LDR has been shown to contribute to the regeneration and functional recovery after transverse peripheral nerve injury (through inducing increased production of VEGF and GAP-43), which advances both the axonal regeneration and myelination. Another mechanism which is possibly involved is preventing neurodegeneration caused by oxidative stress. While high doses can induce reactive oxygen species (ROS) formation, oxidative stress and neuro-inflammation, substantial evidence now indicates that LDR can mitigate tissue damage through antioxidant defenses. Although adult neurogenesis has been reported to be beneficial for the regeneration of  nervous system, some studies demonstrate that neurogenesis increases in AD brains. In spite of these reports, cellular therapy is introduced as a promising strategy for AD, and hence, LDR can affect the proliferation and differentiation of neural stem cells. Although such mechanisms are not fully known yet, it is hoped that this paper would foster further investigation into the mechanisms of this phenomenon, which accordingly improves human health. 
کلیدواژه‌ها
Alzheimer’s Disease؛ Neurohormesis؛ Low Dose Radiation؛ Mechanism
مراجع
  1. Mattson MP. Lifelong brain health is a lifelong challenge: from evolutionary principles to empirical evidence. Ageing Res Rev. 2015;20:37-45. doi: 10.1016/j.arr.2014.12.011. PubMed PMID: 25576651; PubMed Central PMCID: PMC4346441.
  2. Cardoso S, Carvalho C, Correia SC, Seica RM, Moreira PI. Alzheimer’s Disease: From Mitochondrial Perturbations to Mitochondrial Medicine. Brain Pathol. 2016;26:632-47. doi: 10.1111/bpa.12402. PubMed PMID: 27327899.
  3. Smith B, Medda F, Gokhale V, Dunckley T, Hulme C. Recent advances in the design, synthesis, and biological evaluation of selective DYRK1A inhibitors: a new avenue for a disease modifying treatment of Alzheimer’s? ACS Chem Neurosci. 2012;3:857-72. doi: 10.1021/cn300094k. PubMed PMID: 23173067; PubMed Central PMCID: PMC3503344.
  4. Grammas P. Neurovascular dysfunction, inflammation and endothelial activation: implications for the pathogenesis of Alzheimer’s disease. J Neuroinflammation. 2011;8:26. doi: 10.1186/1742-2094-8-26. PubMed PMID: 21439035; PubMed Central PMCID: PMC3072921.
  5. Kwiatkowski D, Sliwinski T. Base excision repair in Alzheimer’s disease. Postepy Hig Med Dosw (Online). 2014;68:976-86. PubMed PMID: 25055036.
  6. Cuttler JM, Moore ER, Hosfeld VD, Nadolski DL. Update on a patient with Alzheimer disease treated with CT scans. Dose-Response. 2017;15:1559325817693167. doi: 10.1177/1559325817693167. PubMed PMID: 28321176; PubMed Central PMCID: PMCPMC5347268.
  7. Cuttler JM, Moore ER, Hosfeld VD, Nadolski DL. Treatment of Alzheimer Disease With CT Scans: A Case Report. Dose Response. 2016;14:1559325816640073-. doi: 10.1177/1559325816640073*. PubMed PMID: 27103883; PubMed Central PMCID: PMC4826954.
  8. Fratiglioni L, Qiu C. Prevention of common neurodegenerative disorders in the elderly. Exp Gerontol. 2009;44:46-50. doi: 10.1016/j.exger.2008.06.006. PubMed PMID: 18620039.
  9. Mortazavi S, Shojaei-Fard M, Haghani M, Shokrpour N, Mortazavi S. Exposure to mobile phone radiation opens new horizons in Alzheimer’s disease treatment. J Biomed Phys Eng. 2013;3:109-12. PubMed PMID: 25505755; PubMed Central PMCID: PMC4204502.
  10. Mortazavi SA, Tavakkoli-Golpayegani A, Haghani M, Mortazavi SM. Looking at the other side of the coin: the search for possible biopositive cognitive effects of the exposure to 900 MHz GSM mobile phone radiofrequency radiation. J Environ Health Sci Eng. 2014;12:75. doi: 10.1186/2052-336X-12-75. PubMed PMID: 24843789; PubMed Central PMCID: PMC4004454.
  11. Schuz J, Waldemar G, Olsen JH, Johansen C. Risks for central nervous system diseases among mobile phone subscribers: a Danish retrospective cohort study. PLoS One. 2009;4:e4389. doi: 10.1371/journal.pone.0004389. PubMed PMID: 19194493; PubMed Central PMCID: PMC2632742.
  12. Arendash GW, Mori T, Dorsey M, Gonzalez R, Tajiri N, Borlongan C. Electromagnetic treatment to old Alzheimer’s mice reverses beta-amyloid deposition, modifies cerebral blood flow, and provides selected cognitive benefit. PLoS One. 2012;7:e35751. doi: 10.1371/journal.pone.0035751. PubMed PMID: 22558216; PubMed Central PMCID: PMC3338462.
  13. Arendash GW, Sanchez-Ramos J, Mori T, Mamcarz M, Lin X, Runfeldt M, et al. Electromagnetic field treatment protects against and reverses cognitive impairment in Alzheimer’s disease mice. J Alzheimers Dis. 2010;19:191-210. doi: 10.3233/JAD-2010-1228. PubMed PMID: 20061638.
  14. Dragicevic N, Bradshaw PC, Mamcarz M, Lin X, Wang L, Cao C, et al. Long-term electromagnetic field treatment enhances brain mitochondrial function of both Alzheimer’s transgenic mice and normal mice: a mechanism for electromagnetic field-induced cognitive benefit? Neuroscience. 2011;185:135-49. doi: 10.1016/j.neuroscience.2011.04.012. PubMed PMID: 21514369.
  15. Zhan X, Jickling GC, Ander BP, Stamova B, Liu D, Kao PF, et al. Myelin basic protein associates with AbetaPP, Abeta1-42, and amyloid plaques in cortex of Alzheimer’s disease brain. J Alzheimers Dis. 2015;44:1213-29. doi: 10.3233/JAD-142013. PubMed PMID: 25697841; PubMed Central PMCID: PMC4422390.
  16. Papuc E, Rejdak K. Does Myelin Play the Leading Role in Alzheimer’s Disease Pathology. J Alzheimers Dis Parkinsonism. 2017;7:2161-0460.1000321.
  17. Tosi R. Nuclear magnetic resonance spectroscopy in the study of neoplastic tissue. New York: Nova Publishers ; 2005.
  18. Jiang B, Zhang Y, Zhao J, She C, Zhou X, Dong Q, et al. Effects of Localized X-Ray Irradiation on Peripheral Nerve Regeneration in Transected Sciatic Nerve in Rats. Radiat Res. 2017;188:455-62. doi: 10.1667/RR14799.1. PubMed PMID: 28796579.
  19. Kurian P, Obisesan TO, Craddock TJA. Oxidative species-induced excitonic transport in tubulin aromatic networks: Potential implications for neurodegenerative disease. J Photochem Photobiol B. 2017;175:109-24. doi: 10.1016/j.jphotobiol.2017.08.033. PubMed PMID: 28865316; PubMed Central PMCID: PMC5610651.
  20. Betlazar C, Middleton RJ, Banati RB, Liu GJ. The impact of high and low dose ionising radiation on the central nervous system. Redox Biol. 2016;9:144-56. doi: 10.1016/j.redox.2016.08.002. PubMed PMID: 27544883; PubMed Central PMCID: PMC4993858.
  21. Eghlidospour M, Ghanbari A, Mortazavi SMJ, Azari H. Effects of radiofrequency exposure emitted from a GSM mobile phone on proliferation, differentiation, and apoptosis of neural stem cells. Anat Cell Biol. 2017;50:115-23. doi: 10.5115/acb.2017.50.2.115. PubMed PMID: 28713615; PubMed Central PMCID: PMC5509895.
  22. Eghlidospour M, Mortazavi SM, Yousefi F, Mortazavi SA. New Horizons in Enhancing the Proliferation and Differentiation of Neural Stem Cells Using Stimulatory Effects of the Short Time Exposure to Radiofrequency Radiation. J Biomed Phys Eng. 2015;5:95-104. PubMed PMID: 26396965; PubMed Central PMCID: PMC4576878.
  23. Bajinskis A, Lindegren H, Johansson L, Harms-Ringdahl M, Forsby A. Low-dose/dose-rate gamma radiation depresses neural differentiation and alters protein expression profiles in neuroblastoma SH-SY5Y cells and C17.2 neural stem cells. Radiat Res. 2011;175:185-92. PubMed PMID: 21268711.
  24. Taupin P. Adult neurogenesis, neural stem cells and Alzheimer’s disease: developments, limitations, problems and promises. Curr Alzheimer Res. 2009;6:461-70. PubMed PMID: 19747153.
  25. Gonzalez-Castaneda RE, Galvez-Contreras AY, Luquin S, Gonzalez-Perez O. Neurogenesis in Alzheimer s disease: a realistic alternative to neuronal degeneration? Curr Signal Transduct Ther. 2011;6:314-9. doi: 10.2174/157436211797483949. PubMed PMID: 22125505; PubMed Central PMCID: PMC3223938.
آمار
تعداد مشاهده مقاله: 873
تعداد دریافت فایل اصل مقاله: 303


سامانه مدیریت نشریات علمی. قدرت گرفته از سیناوب