title: 1950 MHz Electromagnetic Fields Ameliorate Aβ Pathology in Alzheimer's Disease Mice.
abstract: The involvement of radiofrequency electromagnetic fields (RF-EMF) in the neurodegenerative disease, especially Alzheimer's disease (AD), has received wide consideration, however, outcomes from several researches have not shown consistency. In this study, we determined whether RF-EMF influenced AD pathology in vivo using Tg-5xFAD mice as a model of AD-like amyloid β (Aβ) pathology. The transgenic (Tg)-5xFAD and wild type (WT) mice were chronically exposed to RF-EMF for 8 months (1950 MHz, SAR 5W/kg, 2 hrs/day, 5 days/week). Notably, chronic RFEMF exposure significantly reduced not only Aβ plaques, APP, and APP carboxyl-terminal fragments (CTFs) in whole brain including hippocampus and entorhinal cortex but also the ratio of Aβ42 and Aβ40 peptide in the hippocampus of Tg-5xFAD mice. We also found that parenchymal expression of β-amyloid precursor protein cleaving enzyme 1(BACE1) and neuroinflammation were inhibited by RF-EMF exposure in Tg-5xFAD. In addition, RF-EMF was shown to rescue memory impairment in Tg-5xFAD. Moreover, gene profiling from microarray data using hippocampus of WT and Tg- 5xFAD following RF-EMF exposure revealed that 5 genes (Tshz2, Gm12695, St3gal1, Isx and Tll1), which are involved in Aβ, are significantly altered inTg-5xFAD mice, exhibiting different responses to RF-EMF in WT or Tg-5xFAD mice; RF-EMF exposure in WT mice showed similar patterns to control Tg-5xFAD mice, however, RF-EMF exposure in Tg- 5xFAD mice showed opposite expression patterns. These findings indicate that chronic RF-EMF exposure directly affects Aβ pathology in AD but not in normal brain. Therefore, RF-EMF has preventive effects against AD-like pathology in advanced AD mice with a high expression of Aβ, which suggests that RF-EMF can have a beneficial influence on AD.
authors.forename: Ye Ji
authors.initials: YJ
authors.lastname: Jeong
authors.forename: Ga-Young
authors.initials: GY
authors.lastname: Kang
authors.forename: Jong Hwa
authors.initials: JH
authors.lastname: Kwon
authors.forename: Hyung-Do
authors.initials: HD
authors.lastname: Choi
authors.forename: Jeong-Ki
authors.initials: JK
authors.lastname: Pack
authors.forename: Nam
authors.initials: N
authors.lastname: Kim
authors.forename: Yun-Sil
authors.initials: YS
authors.lastname: Lee
authors.affiliation: Division of Radiation Effects, Korea Institute of Radiological & Medical Sciences, Seoul, 139-706, Korea. hjlee@kirams.re.kr.
authors.forename: Hae-June
authors.initials: HJ
authors.lastname: Lee
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D053829:Amyloid Precursor Protein Secretases / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D001362:Avoidance Learning / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D006801:Humans; D055909:Magnetic Field Therapy / Q000379:methods*; D018782:Maze Learning / Q000502:physiology; D008569:Memory Disorders / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D008822:Mice, Transgenic; D017628:Microglia / Q000473:pathology / Q000502:physiology; D009043:Motor Activity / Q000502:physiology; D053764:Presenilin-1 / Q000235:genetics / Q000378:metabolism
chemical_list: C545487:APP protein, human; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C508853:PSEN1 protein, human; D053764:Presenilin-1; D053829:Amyloid Precursor Protein Secretases; D016282:Aspartic Acid Endopeptidases; C509282:Bace1 protein, mouse