title: Electromagnetic treatment to old Alzheimer's mice reverses β-amyloid deposition, modifies cerebral blood flow, and provides selected cognitive benefit.
abstract: Few studies have investigated physiologic and cognitive effects of "long-term" electromagnetic field (EMF) exposure in humans or animals. Our recent studies have provided initial insight into the long-term impact of adulthood EMF exposure (GSM, pulsed/modulated, 918 MHz, 0.25-1.05 W/kg) by showing 6+ months of daily EMF treatment protects against or reverses cognitive impairment in Alzheimer's transgenic (Tg) mice, while even having cognitive benefit to normal mice. Mechanistically, EMF-induced cognitive benefits involve suppression of brain β-amyloid (Aβ) aggregation/deposition in Tg mice and brain mitochondrial enhancement in both Tg and normal mice. The present study extends this work by showing that daily EMF treatment given to very old (21-27 month) Tg mice over a 2-month period reverses their very advanced brain Aβ aggregation/deposition. These very old Tg mice and their normal littermates together showed an increase in general memory function in the Y-maze task, although not in more complex tasks. Measurement of both body and brain temperature at intervals during the 2-month EMF treatment, as well as in a separate group of Tg mice during a 12-day treatment period, revealed no appreciable increases in brain temperature (and no/slight increases in body temperature) during EMF "ON" periods. Thus, the neuropathologic/cognitive benefits of EMF treatment occur without brain hyperthermia. Finally, regional cerebral blood flow in cerebral cortex was determined to be reduced in both Tg and normal mice after 2 months of EMF treatment, most probably through cerebrovascular constriction induced by freed/disaggregated Aβ (Tg mice) and slight body hyperthermia during "ON" periods. These results demonstrate that long-term EMF treatment can provide general cognitive benefit to very old Alzheimer's Tg mice and normal mice, as well as reversal of advanced Aβ neuropathology in Tg mice without brain heating. Results further underscore the potential for EMF treatment against AD.
authors.affiliation: Department of Cell Biology, Microbiology, and Molecular Biology, University of South Florida, Tampa, Florida, United States of America. arendash@cas.usf.edu
authors.forename: Gary W
authors.initials: GW
authors.lastname: Arendash
authors.forename: Takashi
authors.initials: T
authors.lastname: Mori
authors.forename: Maggie
authors.initials: M
authors.lastname: Dorsey
authors.forename: Rich
authors.initials: R
authors.lastname: Gonzalez
authors.forename: Naoki
authors.initials: N
authors.lastname: Tajiri
authors.forename: Cesar
authors.initials: C
authors.lastname: Borlongan
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology / Q000532:radiotherapy*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001831:Body Temperature / Q000528:radiation effects; D002560:Cerebrovascular Circulation / Q000528:radiation effects*; D003071:Cognition / Q000528:radiation effects; D004195:Disease Models, Animal; D004574:Electromagnetic Fields; D006801:Humans; D055909:Magnetic Field Therapy / Q000379:methods*; D018782:Maze Learning / Q000528:radiation effects; D008568:Memory / Q000528:radiation effects; D051379:Mice; D008822:Mice, Transgenic; D008928:Mitochondria / Q000528:radiation effects; D011597:Psychomotor Performance / Q000528:radiation effects
chemical_list: D016229:Amyloid beta-Peptides