Abstract
The aim of the present study was to investigate on the effects of a low-frequency pulsed electromagnetic field (LF-PEMF) in an experimental cell model of Alzheimer's disease (AD) to assess new therapies that counteract neurodegeneration. In recent scientific literature, it is documented that the deep brain stimulation via electromagnetic fields (EMFs) modulates the neurophysiological activity of the pathological circuits and produces clinical benefits in AD patients. EMFs are applied for tissue regeneration because of their ability to stimulate cell proliferation and immune functions via the HSP70 protein family. However, the effects of EMFs are still controversial and further investigations are required. Our results demonstrate the ability of our LF-PEMF to modulate gene expression in cell functions that are dysregulated in AD (i.e., BACE1) and that these effects can be modulated with different treatment conditions. Of relevance, we will focus on miRNAs regulating the pathways involved in brain degenerative disorders.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder with irreversible progression that primarily affects the hippocampal and neocortical regions of the brain
Our results demonstrate the ability of our low-frequency pulsed electromagnetic field (LF-pulsed electromagnetic fields (PEMFs)) to modulate gene expression in cell functions that are dysregulated in AD (i.e., BACE1) and that these effects can be modulated with different treatment conditions
extracellular signal-regulated kinase (ERK) activity contributes to the synaptic plasticity; ERK cascade signals act with a regulatory role on the AMPA glutamate receptor (AMPAR), a non-NMDA type ionotropic transmembrane receptor for glutamate characterized by four types of subunits called GRIA [67]
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder with irreversible progression that primarily affects the hippocampal and neocortical regions of the brain. Since the incidence of AD increases in the elderly and with the lengthening of human life, this disease is becoming one of the major health problems associated with aging [1]. The major microscopic abnormalities of AD, which form the basis of the histologic diagnosis, are β-amyloid (Aβ) plaques and neurofibrillary degeneration (tangles). There are progressive and eventually severe neuronal loss, synaptic loss, and reactive gliosis in the same regions that bear the burden of the plaques and tangles. The involvement of the hippocampus and amygdale in the early phases of AD causes synaptic dysfunctions, such as the block of long-term potentiation (LTP), with consequent damage of the processes of learning and memory [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
