Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice

Neurotoxicology. 2016 Mar:53:290-300. doi: 10.1016/j.neuro.2016.02.012. Epub 2016 Mar 2.

Abstract

Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its effects on cognitive deficits in Alzheimer's disease (AD) have remained under debate. Moreover, the influence of ELF-MF on hyperphosphorylated tau, which is one of the most common pathological hallmarks of AD, has not been reported to date. Therefore, transgenic mice (3xTg) were used in the present study. 3xTg mice, which express an APP/PS1 mutation combined with a tau (P301L) mutation and that develop cognitive deficits at 6 months of age, were subjected to ELF-MF (50Hz, 500μT) exposure or sham exposure daily for 3 months. We discovered that ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice. The protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice. Furthermore, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac. We are the first to report that exposure to ELF-MF can attenuate tau phosphorylation. These findings suggest that ELF-MF exposure could act as a valid therapeutic strategy for ameliorating cognitive deficits and attenuating tau hyperphosphorylation in AD.

Keywords: Alzheimer’s disease; Cognitive; ELF-MF; Tau phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / complications*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / radiotherapy
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Apoptosis / genetics
  • Apoptosis / radiation effects
  • Cognition Disorders / etiology*
  • Cognition Disorders / therapy*
  • Conditioning, Psychological / physiology
  • Conditioning, Psychological / radiation effects
  • Cyclin-Dependent Kinase 5 / genetics
  • Cyclin-Dependent Kinase 5 / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Radiation
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / radiation effects
  • Glycogen Synthase Kinase 3 beta / genetics
  • Glycogen Synthase Kinase 3 beta / metabolism
  • Humans
  • Magnetic Field Therapy / methods*
  • Maze Learning / physiology
  • Maze Learning / radiation effects
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mutation / genetics
  • Phosphorylation / radiation effects
  • Presenilin-1 / genetics
  • Reactive Oxygen Species / metabolism
  • tau Proteins / genetics
  • tau Proteins / metabolism*

Substances

  • Amyloid beta-Protein Precursor
  • PSEN1 protein, human
  • Presenilin-1
  • Reactive Oxygen Species
  • tau Proteins
  • Cyclin-Dependent Kinase 5
  • Glycogen Synthase Kinase 3 beta
  • Cdk5 protein, mouse