title: 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?
abstract: We have recently reported that long-term exposure to high frequency electromagnetic field (EMF) treatment not only prevents or reverses cognitive impairment in Alzheimer's transgenic (Tg) mice, but also improves memory in normal mice. To elucidate the possible mechanism(s) for these EMF-induced cognitive benefits, brain mitochondrial function was evaluated in aged Tg mice and non-transgenic (NT) littermates following 1 month of daily EMF exposure. In Tg mice, EMF treatment enhanced brain mitochondrial function by 50-150% across six established measures, being greatest in cognitively-important brain areas (e.g. cerebral cortex and hippocampus). EMF treatment also increased brain mitochondrial function in normal aged mice, although the enhancement was not as robust and less widespread compared to that of Tg mice. The EMF-induced enhancement of brain mitochondrial function in Tg mice was accompanied by 5-10 fold increases in soluble Aβ1-40 within the same mitochondrial preparations. These increases in mitochondrial soluble amyloid-β peptide (Aβ) were apparently due to the ability of EMF treatment to disaggregate Aβ oligomers, which are believed to be the form of Aβ causative to mitochondrial dysfunction in Alzheimer's disease (AD). Finally, the EMF-induced mitochondrial enhancement in both Tg and normal mice occurred through non-thermal effects because brain temperatures were either stable or decreased during/after EMF treatment. These results collectively suggest that brain mitochondrial enhancement may be a primary mechanism through which EMF treatment provides cognitive benefit to both Tg and NT mice. Especially in the context that mitochondrial dysfunction is an early and prominent characteristic of Alzheimer's pathogenesis, EMF treatment could have profound value in the disease's prevention and treatment through intervention at the mitochondrial level.
authors.affiliation: Department of Cell Biology, University of South Florida, FL 33620, USA.
authors.forename: N
authors.initials: N
authors.lastname: Dragicevic
authors.forename: P C
authors.initials: PC
authors.lastname: Bradshaw
authors.forename: M
authors.initials: M
authors.lastname: Mamcarz
authors.forename: X
authors.initials: X
authors.lastname: Lin
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: C
authors.initials: C
authors.lastname: Cao
authors.forename: G W
authors.initials: GW
authors.lastname: Arendash
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000704:Analysis of Variance; D000818:Animals; D001831:Body Temperature / Q000235:genetics; D001921:Brain / Q000473:pathology / Q000528:radiation effects / Q000648:ultrastructure*; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D006801:Humans; D055909:Magnetic Field Therapy / Q000379:methods*; D053078:Membrane Potential, Mitochondrial / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D008928:Mitochondria / Q000528:radiation effects*; D009154:Mutation / Q000235:genetics; D010446:Peptide Fragments / Q000378:metabolism; D053764:Presenilin-1 / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: C545487:APP protein, human; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C508853:PSEN1 protein, human; D010446:Peptide Fragments; D053764:Presenilin-1; D017382:Reactive Oxygen Species; C075222:amyloid beta-protein (1-42); D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV