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Abstract

The aim of this work is to present the current knowledge about the possible participation of electromagnetic fields in the occurrence and also in treatment of neurodegenerative diseases. The literature data indicate both the negative and positive effects of electromagnetic fields and not allow to draw unambiguous conclusions. Undoubtedly, the topic is still open and needs further intensive research to finally assess the mechanism of action of the electromagnetic field on neurodegenerative diseases.
PRZEGLĄD ELEKTROTECHNICZNY, ISSN 0033-2097, R. 95 NR 1/2019 129
Joanna WYSZKOWSKA1, Milena JANKOWSKA1, Piotr GAS2
Nicolaus Copernicus University (1), AGH University of Science and Technology (2)
doi:10.15199/48.2019.01.33
Electromagnetic Fields and Neurodegenerative Diseases
Abstract. The aim of this work is to present the current knowledge about the possible participation of electromagnetic fields in the occurrence and
also in treatment of neurodegenerative diseases. The literature data indicate both the negative and positive effects of electromagnetic fields and not
allow to draw unambiguous conclusions. Undoubtedly, the topic is still open and needs further intensive research to finally assess the mechanism of
action of the electromagnetic field on neurodegenerative diseases.
Streszczenie. Celem niniejszej pracy jest przedstawienie aktualnej wiedzy o możliwym udziale pól elektromagnetycznych w występowaniu oraz
w leczeniu chorób neurodegeneracyjnych. Dane literaturowe wskazują zarówno na negatywny, jak i pozytywny wpływ pól elektromagnetycznych
i nie pozwalają na wyciągnięcie jednoznacznych wniosków. Niewątpliwie temat jest nadal otwarty i wymaga dalszych intensywnych badań, aby
ostatecznie ocenić mechanizm działania pola elektromagnetycznego na choroby neurodegeneracyjne. (Pola elektromagnetyczne i choroby
neurodegeneracyjne)
Keywords: electromagnetic fields, nervous system, neurodegenerative diseases, transcranial magnetic stimulation (TMS).
Słowa kluczowe: pola elektromagnetyczne, układ nerwowy, choroby neurodegeneracyjne, przezczaszkowa stymulacja mózgu (TMS).
Introduction
The increasing number of artificial sources of electro-
magnetic fields (EMFs) raises concern about its impact on
human health. Beside many beneficial and therapeutic
applications of EMFs [1], there are more and more publica-
tions describing the unfavourable effect of the EMFs expo-
sure on humans and mostly pointing on the deterioration of
well-being, disruption of the nervous system functions or
the cancer occurrence. Recently, there have also appeared
articles indicating the relationship between the higher
incidence of neurodegenerative diseases and the increased
exposure to EMFs [2]–[4]. However, the published results
are not unequivocal and often contradictory. Researchers
try to define a mechanism that could explain the impact of
EMFs exposure on the increased incidence of neuro-
degenerative diseases, suggesting the participation of,
among others, oxidative stress. Nevertheless, further re-
search is needed to thoroughly explain the mechanism of
action of the EM field on the central nervous system and to
explain the potential relationship with neurodegenerative
diseases. In this paper, neurodegenerative diseases such
as Alzheimer's disease (AD), Parkinson's disease (PD),
amyotrophic lateral sclerosis (ALT) and multiple sclerosis
(MS) will be briefly presented. Next, the relationship be-
tween the incidence of neurodegenerative diseases and the
EMFs exposure will be discussed. Also an examples of
usage of EM fields in the treatment of neurodegenerative
diseases will be described at the end.
A brief description of neurodegenerative diseases
Neurodegeneration is the progressive loss of structure or
function of neurons, including death of neurons. There are
several hundred neurodegenerative diseases (NDD), and
the main difficulty in their classification lies in the fact that
their symptoms may coincide with each other. An additional
issue in the classification of neurodegenerative diseases is
the fact that in many neurodegenerative diseases several
areas of the brain are affected (e.g. in multi-system loss)
which lead to unspecific clinical picture, moreover different
combinations of brain changes may give different clinical
symptoms. In addition, the neurodegenerative process itself
can affect different areas of the brain at the beginning,
giving symptoms that differ from those typical for a given
disease. Despite these difficulties, the most common cate-
gorization of neurodegenerative disorders is based on: the
main clinical features or the topography of the prevailing
changes, often both are taken into account [5].
Alzheimer's disease
Alzheimer's disease (AD) is a syndrome of neuro-
degenerative disorders leading to dementia. The AD brain
is characterized by the presence of 2 classes of abnormal
structures, extracellular amyloid plaques and intraneuronal
neurofibrillary tangles (NFT). The soluble building blocks of
these structures are amyloid-β (Aβ) peptides for plaques
and tau proteins for tangles. Amyloid-β peptides are proteo-
lytic fragments of the transmembrane amyloid precursor
protein, whereas tau protein is a brain-specific, axon-
enriched microtubule-associated protein [6]. It has been
proven that Aβ stimulates the process of apoptosis, or pro-
grammed cell death [7, 8]. The behavioural symptoms of
AD correlate with the accumulation of plaques and tangles,
whose a direct consequences are damage and destruction
of synapses that mediate memory and cognition. Synapse
loss can be caused by the failure of live neurons to maintain
functional axons and dendrites or by neuron death [6].
Senile plaques have a negative effect on neurons and
damage them as a result of unexplained mechanisms, it is
suspected that they disturb ion balance in nerve cells which
results in damage to the nerve signal conduction and al-
tered calcium channel activity in synapses. In turn, the
intraneuronal presence of the NFT primarily reduces axonal
flow and slows down the metabolism of the neuron to ulti-
mately lead to cell death [7]. In Alzheimer's disease there is
a significant decrease in the concentration of acetylcholine,
an important neuro-transmitter that participates in memory
processes, and also a decrease in the concentration of
serotonin, noradrenaline and dopamine.
Scientists don’t yet fully understand what causes AD
in most people. The molecular basis of Alzheimer's disease
is associated with mutations in three genes (15% of cases)
in early-onset Alzheimer's disease . Late-onset Alzheimer's
arises from a complex series of brain changes that occur
over decades. The causes probably include a combination
of genetic, environmental, and lifestyle factors as: 1) age,
which is one of the most important factors in Alzheimer's
disease; 2) sex; 3) low level of education or lack of edu-
cation; 4) serious head injury or repeated minor injuries; 5)
myocardial ischemia; 6) advanced maternal age, increases
the probability of occurrence of Alzheimer's disease in a
child, and 7) stressors. The association of AD with immune
disorders is also suspected. In the ethology of Alzheimer's
disease, it is more and more often indicated on the part of
oxidative stress, which leads to disturbances of the prooxi-
dative and antioxidative balance [9].
130 PRZEGLĄD ELEKTROTECHNICZNY, ISSN 0033-2097, R. 95 NR 1/2019
Multiple sclerosis
Multiple sclerosis (MS) is a condition that affects the
central nervous system (the brain and the spinal cord) in a
variety of ways. Scientists don’t know what causes MS but
they do know that it provokes an “auto-immune reaction”. In
this ‘auto-immune attack’ the body fails to recognise its own
tissue (in this case, myelin tissue) as part of itself and the
immune system swings into action to destroy it. In MS, the
myelin sheath becomes inflamed. Sometimes the inflamma-
tion dies down, but if it continues, the myelin is damaged
and a scar forms. Scientists have called these scars
‘plaques’ or ‘sclerosis’ (from the Greek word for scar). This
process is called demyelination (FS-MS). Demyelination
causes slowing or loss of nerve conduction [10, 11]. Multi-
ple sclerosis can cause damage in any structure of the
central nervous system, which is the reason why the course
of the disease is very diverse in each person and depends
on the location of demyelinating lesions [11]. The onset of
the disease may not be noticeable, and the symptoms of
the disease may be transient and mild. Initial symptoms in-
clude: 1) sensory disorder on the limbs or face; 2) paresis of
a pyramidal limb; 3) impaired motor coordination; 4) total or
partial failure to see 5) double vision episodes; 6) impair-
ment; 7) instability of gait; 8) disturbance of balance. One of
the most common disorders in the case of MS is visual
disturbances. The spectrum of symptoms is very wide and
can affect almost every part of our body, which significantly
worsens the quality of patient's life [12].
Parkinson's disease
Parkinson's disease (PD) is a progressive neuro-
degenerative movement disorder associated with the loss of
cells in various parts of the brain, including a region called
the substantia nigra–one of the main producer of dopamine
in human brain. Loss of dopamine causes neurons to fire
without normal control, leaving patients less able to direct or
control their movement. The exact cause of Parkinson's
disease is unknown, although research points to a combi-
nation of genetic and environmental factors. The single
biggest risk factor for Parkinson's disease is advancing age.
Men have a somewhat higher risk than women. The primary
symptoms of Parkinson's disease are all related to voluntary
and involuntary motor function and usually start on one side
of the body. Other symptoms can include: 1) Cognitive
impairment; 2) Mood disorders; 3) Sleep difficulties; 4) Loss
of sense of smell, called hyposmia; 5) Constipation, speech
and swallowing problems [13]. Increasing evidence sug-
gests that oxidative stress is responsible for cell loss in
the substantia nigra [14, 15]. The substantia nigra of PD
patients exhibit increased levels of oxidized lipids [16],
proteins and DNA [17] and decreased levels of reduced
glutathione (GSH) [18].
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) is a group of rare
neurological diseases that mainly involve the nerve cells
(neurons) responsible for controlling voluntary muscle
movement. ALS is caused by gradual deterioration (de-
generation) and death of motor neurons which initiate and
provide vital communication links between the brain and the
voluntary muscles [19]. Messages from motor neurons in
the brain (called upper motor neurons) are transmitted to
motor neurons in the spinal cord and to motor nuclei of
brain (called lower motor neurons) and from the spinal cord
and motor nuclei of brain to a particular muscle or muscles.
In ALS, both the upper motor neurons and the lower motor
neurons degenerate or die, and stop sending messages to
the muscles. Unable to function, the muscles gradually
weaken, start to twitch (it is called fasciculation), and waste
away (atrophy). Eventually, the brain loses its ability to
initiate and control voluntary movements [20].
Early symptoms of ALS usually include muscle weak-
ness or stiffness. Gradually all muscles under voluntary
control are affected, and individuals lose their strength and
the ability to speak, eat, move, and even breathe.
In searching for the cause of ALS, researchers are also
studying the impact of environmental factors. The number
of possible causes is investigated such as exposure to toxic
or infectious agents, viruses, physical trauma, diet, and
behavioural and occupational factors.
One of the suggested mechanisms is oxidative stress,
which increases the permeability of the mitochondrial mem-
brane and the release of calcium ions. This in turn leads to
the death of the cell, and thus the motor neurons of the
brain, trunk and spinal cord cortex [19].
Electromagnetic field and neurodegenerative diseases
Researchers are looking for external factors that are
responsible for developing the neurodegenerative diseases.
Several recent reports indicate that exposure to electric and
magnetic fields may be associated with increased risk of
NDD, and the most importance is attached to occupational
exposure. It has been strengthened in the last decade, for
example in the following studies [21]–[25].
Based on an analysis of the death certificates, it was
found that among people professionally exposed to electro-
magnetic fields (e.g. power plant operators) there is higher
ratio of death because of neurodegenerative diseases than
in other professional groups [26]. However, occurrence of
Alzhaimer’s disease and amyotrophic lateral sclerosis was
stronger associated with electric and magnetic field
exposition than Parkinson’s disease. In similar study [27]
the higher mortality rate because of Alzheimer’s disease
in men exposed to magnetic field is found, but in contrast
to the study [26] myotrophic lateral sclerosis deaths was not
associated with magnetic field exposure. The increase risk
of Alzheimer’s disease was also confirmed in an extensive
meta-analysis [22]. Study [28] seems to confirm evidence of
a relationship between occupational EMF exposure and AD,
in which an increased incidence of Alzheimer's disease in
males before the age of 75 exposed to EM fields at work,
was concluded. Researchers also provided analysis of
death rate of people lived in neighbourhood of the high-
voltage line. Authors observed increased mortality due to
neurodegenerative diseases in particular Alzheimer's dis-
ease in residents living nearby (50 m or less) 220–380 kV
power lines [3].
In contrary, study [29] in huge analysis based on 30,631
persons does not observed correlation between Alzheimer’s
diseases and occupational exposure to electromagnetic
fields.
In most available data the association between Par-
kinson disease and electromagnetic field exposure is not
observed [22, 29, 30]. However, in [22] the authors found
an increased incidence of PD as a result of electromagnetic
fields exposure.
Although the publications on the subject of association
of EM field and neurodegenerative diseases are quite
numerous, it is important to note that all those analysis are
based on death certificates and medical documentation
only. Many external factors can be important in determining
the risk of NDD in different professional groups, such as the
severity of work, physical or mental work, and lifestyle.
People subjected to occupational exposition of EMF are
predominantly physical worker. What is more, the data from
death certificates mostly concerns people who lived and
worked in the ’70, ’80 and ’90. Such a data may lead to
conclusions that are inadequate to the present days.
PRZEGLĄD ELEKTROTECHNICZNY, ISSN 0033-2097, R. 95 NR 1/2019 131
In in vivo and in vitro studies conducted in [3] it was
shown that EM fields can cause mild oxidative stress
(increase in ROS (reactive oxygen species) and changes
in antioxidant levels) and is involved in anti-inflammatory
processes (reduction of proinflammaory cytokines and in-
crease in anti-inflammatory cytokines). The increase in the
level of pro-inflammatory cytokines after exposure to EMF
(1–7 mT, and 50 Hz) was also demonstrated in experiments
on rats [31].
The participation of inflammatory processes may lead to
the activation of microglia and the intensification of oxidative
stress caused by the explosion of electrons. Inflammation in
the central nervous system often occurs in the case of
Alzheimer's disease, Parkinson's disease or in the case of
chronic neurological disorders. The cascade of inflamma-
tion is initiated by microglia and astrocytes of the central
nervous system. The fact that microglia are active in the
aging brain and the occurrence of natural neuronal death
indicates that the interaction between neuron and glial
cells play a significant role in controlling the inflammatory
response of the central nervous system [32, 33]. As it was
already mentioned, EM field exposure can lead to oxidative
stress in the body. In the review [34], author indicates, that
the exposure to EMFs (50 Hz, 0.1–1.0 mT) can cause redox
reactions and the induction of oxidative stress in the mouse
brain. This increases the level of free radicals, which leads
to oxidative damage to the lipids in the brain of mice
and rats. In the experimental model of the rat, which was
exposed to the 50 Hz EM field (100 and 500 μT), there was
a strong toxic effect disturbing the antioxidant effect. It was
shown that exposure to 50 Hz frequency electromagnetic
field (0.1–1.0 mT), affects the antioxidant capacity of en-
zymes in both the brain of young and old rats. However,
in older rats, a large decrease in all major anti-oxidative
enzymes was observed, thus indicating an age-dependent
greater susceptibility to induction of oxidative stress as a
result of exposure to the EM field [34].
Electromagnetic fields in the treatment of neuro-
degenerative diseases
Despite the negative influence of electromagnetic fields
on the CNS, its positive effects is noticeable and is used in
the therapy of many neurodegenerative diseases as shown
in the following studies [35]–[37].
Magnetotherapy
Magnetotherapy involves the use of a magnetic field
with a magnetic flux density value from 0.1 to 20 mT, and a
frequencies up to 100 Hz. Its action on the nervous system
consists in improving the metabolism of nerve cells, blood
supply to the brain, intensification of synaptic reorganization
processes or analgesic effects, in patients with MS
receiving magnetotherapy, reduction in muscle tremor,
nystagmus, pain, dizziness and better urination control
is observed. It was also proved that after magnetotherapy
treatment, the functions of damaged cranial nerves were
restored. In the case of MS, retrobulbar optic neuritis is
common, and after magnetotherapy, visual acuity was
improved [38]–[40]. It is worth noting that researchers still
design novel applicators for magnetotherapy and their
performance is tested both by computer simulation and
experiments [41]–[43]. An important problem is also human
exposure to electromagnetic fields near various magneto-
therapeutic devices [44].
Magnetostimulation
Magnetostimulation is a procedure in which a magnetic
field is used (the magnetic flux density values are from 1 pT
to 100 µT and the basic frequency course ranges from a
few to 3000 Hz). Basic waveforms are modulated in such a
way that their envelopes have a waveform with frequencies
from a few to 100 Hz. The therapeutic cycle should include
14 daily treatments. In selected cases, it is advisable to re-
peat the cycle after 4 weeks [40, 45]. Magnetostimulation
affects the limbic system and the cerebral cortex. Particular
indications for magnetostimulation are depression, fatigue
syndrome, cognitive disorders and circadian rhythms.
Magnetostimulation reduces the symptoms of depression,
improves the mood of patients, reduce anxiety. The results
of clinical trials confirmed the high therapeutic efficacy of
magneto-stimulation using weak variable magnetic fields in
the treatment of neurotic symptoms in the course of multiple
sclerosis, Parkinson's disease and Alzheimer's disease
[46]–[49]. In the paper [50], the authors described positive
effects of treatment with EMFs of a patient with chronic
progressive MS. Regularly weekly transcortical treatments
with pulsed EMFs (4.2 Hz, and 7.5 pT) improved mental
functions, returned the strength in the upper extremities,
and recovered a trunk control. With prolonged treatment the
return of more hip functions and recovery of motor functions
in legs were observed. Also about 80% of functions in the
upper limbs and hands was regained.
Transcranial magnetic stimulation (TMS)
In In the 1980’s, researchers introduced TMS into medi-
cal practice as a diagnostic tool in neurology for exploring
brain function, and for treating neurological disorders such
as multiple sclerosis, Parkinson's disease, Alzheimer's dis-
ease, autism, Asperger’s disorder, substance addictions,
neuropathic pain, and schizophrenia [50].
This form of stimulation involves the use of a magnetic
field of 2 T and a very short pulse duration (100-200 μs)
with a frequency from 1 to 100 Hz to induce an electric field
in the brain [51, 52]. Therapeutic potential lies in repetitive
stimulation modulating cortical excitability which also has
behavioural consequences. TMS uses EM induction to elec-
trically influence nearby cells. Strong effects can depolarize
neurons and trigger action potentials. Low intensity TMS
mostly stimulate low-threshold inhibitory interneurons,
whereas higher intensities excite axons of neurons [53, 54].
This method allows to stimulate the brain areas located up
to 2 cm from its surface [40, 50]. Moreover, an induced
electric field might cause several changes in metabolism,
neurotransmitters release, and induction of gene expression
[47]. TMS holds great potential as a tool for understanding
how the brain works, correcting its dysfunctions and even
augmenting its abilities [37].
TMS replaced the painful transcranial electrical stimu-
lation, due to the deeper penetration of the magnetic pulse
through resistant electrical tissues, this method ensures
painlessness and non-invasiveness. The use of TMS to
assess the functional status of the central motor neuron
enabled a better understanding of the neurophysiological
basis of Parkinson's disease. In patients with PD, attempts
were made to use rTMS (repetitive TMS – magnetic stimu-
lation with a series of pulses), at a frequency of 0.2, 1 to
5 Hz, which resulted in improved motor function in these
patients. In patients with MS, the use of TMS resulted in
lowering the amplitude of reflexes and muscle contraction in
the lower limb, scientists explain this fact with plastic lesions
in the spinal cord under the influence of TMS. Recent
studies have indicated that high frequency repetitive TMS
has significant therapeutic effect on cognitive function in
patients with mild to moderate Alzheimer’s diseases [55]–
[57]. What is interesting, the TMS issue is successfully
analysed in numerous computer studies [58]–[60].
132 PRZEGLĄD ELEKTROTECHNICZNY, ISSN 0033-2097, R. 95 NR 1/2019
Summary
The aim of this work was to present current knowledge
about the participation electromagnetic fields in the oc-
currence and treatment of neurodegenerative diseases
Neurodegenerative diseases are the increasingly common
problem of today's society. This is due to the fact that every
year the number of cases of these diseases increase.
Currently, in the era of rapid technical progress, people are
increasingly surrounded by devices emitting an EM field.
Researchers are trying to link these two issues. The thesis
that the EM field increases the risk of neurodegenerative
diseases generates much lack of clarity.
In the case of Parkinson's disease and multiple sclero-
sis, there is not enough research to determine whether
EMFs affects the development of these diseases. However,
some scientists cast a shadow of uncertainty claiming that
the electromagnetic field contributes to the formation of
oxidative stress in the body and in this way to the oc-
currence of these diseases. However, in the case of
Alzheimer's disease and amyotrophic lateral sclerosis, there
are many studies indicating the participation of the EMF in
the development of these diseases. Although many results
are not consistent, there is an increased risk of AD
developing in men, but it is not found in women. The
uncertainties in the results of research probably result from
insufficient methodology, they are based mainly on death
certificates.
It can be assumed that EMFs affects the occurrence of
neurodegenerative diseases indirectly, EMFs causes oxida-
tive stress in the body and is involved in the anti-
inflammatory process, and these processes may contribute
to the development of neurodegenerative diseases. The
lack of a sufficient number of tests and literature data does
not allow to draw unambiguous conclusions regarding the
influence of the electromagnetic field on neurodegenerative
diseases.
As it was briefly described above EMFs could be a
useful also as therapy for any brain disorder involving
dysfunctional behaviour in a neural circuit. EMFs have been
tried to employ as a treatment for disorder, schizophrenia,
Parkinson’s, dystonia (involuntary muscle contractions),
chronic pain and epilepsy.
For most of these cases, only a few inconclusive studies
currently exist. Nevertheless, interest remains high among
researchers who continue of using safe magnetic fields to
turn specific brain regions on and off [36]. Undoubtedly,
further intensive research is needed to finally assess the
mechanism of action of the electromagnetic field on
neurodegenerative diseases.
Acknowlegments
The authors would like to thank Donovan Kelorii (LSBA,
CELTA) for constructive criticism and copy editing of the
manuscript.
Authors: dr Joanna Wyszkowska, Nicolaus Copernicus University,
Faculty of Biology and Environmental Protection, Department of
Biophysics ul. Lwowska 1, 87-100 Toruń, E-mail:
joanna.wyszkowska@umk.pl;
mgr Milena Jankowska, Nicolaus Copernicus University, Faculty of
Biology and Environmental Protection, Department of Biophysics,
E-mail: milena.jankowska@umk.pl;
dr inż. Piotr Gas, AGH University of Science and Technology,
Department of Electrical and Power Engineering, al. Adama
Mickiewicza 30, 30-059 Kraków, E-mail: piotr.gas@agh.edu.pl.
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... However, our understanding of the benefits of magnetic stimulation (MS) for patients with neurological disorders is incomplete (especially neurodegenerative diseases). The literature presents both positive and negative outcomes for this type of treatment [19]. There have been only a few studies on the clinical effects of ELFMFs published in well-known journals in the field [16]. ...
... Res. Public Health 2022,19, 4012 ...
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There is an ongoing debate on the benefits of magnetic stimulation in neurological disorders. Objectives: We aimed to evaluate the influence of magnetic stimulation on blood oxygenation of the motor cortex using functional near-infrared spectroscopy (fNIRS). Methods: A total of 16 healthy volunteer participants were subjected to four protocols. In the first two protocols, the participants remained at rest without (and then with) magnetic stimulation. In the next two protocols, motor cortex stimulation was achieved using a finger-tapping task, with and without magnetic stimulation. Changes in blood oxygenation levels within the motor cortex were recorded and analysed. Results: No characteristic changes in the blood oxygenation level-dependent responses were observed in resting participants after magnetic stimulation. No statistically significant difference was observed in the amplitude of the fNIRS signal before and after magnetic stimulation. We observed characteristic blood oxygenation level-dependent responses after the finger-tapping task in the second protocol, but not after magnetic stimulation. Conclusions: Although we did not observe any measurable effect of the magnetic field on the haemodynamic response of the motor cortex, understanding the mechanism(s) of magnetic stimulation may be important. Additional, detailed studies are needed to prove or negate the potential of this medical procedure.
... The increasing number of man-made sources of electromagnetic field (EMF) raises interest in occupational groups about its impact on human health, especially concerning the high level of exposure. While there are some beneficial and therapeutic applications of EMF, there are more and more publications devoted to the unfavourable effects of EMF exposure on humans, mostly pointing to the deterioration of their well-being, disruptions to the functions of the nervous system, or linking it to the occurrence of cancer [1][2][3][4][5][6][7][8]. ...
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This work presents the current state of knowledge about the possible contributory influence of the electromagnetic field on the occurrence of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis. Up-to-date literature indicates both favourable and adverse effects of electromagnetic exposure on human health, making it difficult to come to valid and unambiguous conclusions. The epidemiological data analysis from the World Health Organization statistics shows a substantial rise in neurological mortality compared with rises in total populations in developed countries over a mere 15-year period. The largest of the analysed countries produced odds ratios of >100%. The contribution of electromagnetic exposure to the incidence of neurodegenerative diseases is still undoubtedly open to discussion, and it requires further in-depth research to assess the action mechanism of electromagnetic fields in neurodegenerative diseases. The limitations of research published hitherto and the problem of drawing unequivocal conclusions are also in focus.
... Recently the WHO's International Agency for Research on Cancer listed radio-frequency electromagnetic fields (RF-EMFs), ranging from 10 MHz to 300 GHz, as potentially carcinogenic (Baan et al., 2011). On the other hand, an increasing number of studies reported EMFs beneficial role in the treatment of numerous chronic diseases, such as cancer, mood disorders and many forms of neurodegeneration (Jimenez et al., 2018;Martiny et al., 2010;Wyszkowska et al., 2019), paving the way for the therapeutic use of magnetic-field based techniques, such as Transcranial Magnetic Stimulation and Pulsed Electromagnetic Field (PEMF) stimulation (Hallett, 2000;Markov, 2007). ...
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Biological effects of electromagnetic fields (EMFs) have previously been identified for cellular proliferation and changes in expression and conduction of diverse types of ion channels. The major effect elicited by EMFs seems to be directed toward Ca2+ homeostasis. This is particularly remarkable since Ca2+ acts as a central modulator in various signaling pathways, including, but not limited to, cell differentiation and survival. Despite this, the mechanisms underlying this modulation have yet to be unraveled. Here, we assessed the effect of EMFs on intracellular [Ca2+], by exposing HEK 293 cells to both radio‐frequency electromagnetic fields (RF‐EMFs) and static magnetic fields (SMFs). We detected a constant and significant increase in [Ca2+] subsequent to exposure to both types of fields. Strikingly, the increase was nulled by administration of 10 μM Thapsigargin, a blocker of sarco/endoplasmic reticulum Ca2+‐ATPases (SERCAs), indicating the involvement of the endoplasmic reticulum (ER) in EMF‐related modulation of Ca2+ homeostasis.
... 1,3,4 Epidemiological studies reported a significant association between exposure to ELF-EMF and the development of childhood leukemia, 5,6 and in 2011, WHO's International Agency for Research on Cancer highlighted the possible carcinogenic effect of RF-EMFs. 7 However, EMFs have also been extensively used in the treatment of many forms of neoplasia 8 and neurodegenerative diseases, 9 highlighting a possible beneficial use of these fields as therapeutic treatments for diverse chronic diseases. The effects on the central nervous system (CNS) appear to be particularly relevant, as the CNS is reliant on many voltage-dependent processes. ...
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Many aspects of chemistry and biology are mediated by electromagnetic field (EMF) interactions. The central nervous system (CNS) is particularly sensitive to EMF stimuli. Studies have explored the direct effect of different EMFs on the electrical properties of neurons in the last two decades, particularly focusing on the role of voltage‐gated ion channels (VGCs). This work aims to systematically review published evidence in the last two decades detailing the effects of EMFs on neuronal ion channels as per the PRISM guidelines. Following a predetermined exclusion and inclusion criteria, 22 papers were included after searches on three online databases. Changes in calcium homeostasis, attributable to the voltage‐gated calcium channels, were found to be the most commonly reported result of EMF exposure. EMF effects on the neuronal landscape appear to be diverse and greatly dependent on parameters, such as the field's frequency, exposure time, and intrinsic properties of the irradiated tissue, such as the expression of VGCs. Here, we systematically clarify how neuronal ion channels are particularly affected and differentially modulated by EMFs at multiple levels, such as gating dynamics, ion conductance, concentration in the membrane, and gene and protein expression. Ion channels represent a major transducer for EMF‐related effects on the CNS. This work aims to systematically review published evidence in the last two decades detailing the effects of electromagnetic fields (EMFs) on neuronal ion channels as per the PRISM guidelines. Here, we systematically clarify how neuronal ion channels are particularly affected and differentially modulated by EMFs at multiple levels, such as gating dynamics, ion conductance, concentration in the membrane, and gene and protein expression.
... Nevertheless, several studies have reported that EMF could affect brain function leading to mental and various types of neurological disorders (Pall, 2016;Terzi, Ozberk, Deniz, & Kaplan, 2016;Wyszkowska, Jankowska, & Gas, 2019). Moreover, in our previous studies, we have shown the deleterious effects of exposure to 900 MHz radiofrequency waves (RFW) on brain function including memory impairment and oxidative damage (Akbari, Jelodar, & Nazifi, 2014;Azimzadeh et al., 2018). ...
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Advances in telecommunication and their broad usage in the community have become a great concern from the health aspect. The object of the present study was to examine the effects of exposure to 900 MHz RFW on brain Iron (Fe), Copper (Cu), Zinc (Zn) and Manganese (Mn) concentration, and the protective role of pre‐treatment of vitamin E on mentioned elements homoeostasis. Twenty adult male Sprague–Dawley rats (200 ± 20 g) randomly were divided into four groups. Control group (without any exposure, received distilled water), treatment control group (orally received 250 mg/kg BW/d vitamin E), treatment group (received 250 mg/kg BW/d vitamin E and exposed to 900 MHz RFW) and sham‐exposed group (exposed to 900 MHz RFW). Animals (with freely moving in the cage) were exposed to RFW for 30 consecutive days (4 hr/day). The levels of the above mentioned elements in the brain tissue were determined on the last day using atomic absorption spectrophotometry. Exposure to 900 MHz RFW induced a significant increase in the Fe, Cu, Mn levels and Cu/Zn ratio accompanied by a significant decrease in Zn level in the sham‐exposed group compare to control group. Vitamin E pre‐treatment improved the level of Fe, Cu, Mn and Cu/Zn ratio, except in the Zn concentration. Exposure to 900 MHz RFW caused disrupted trace elements homoeostasis in the brain tissue and administration of vitamin E as an antioxidant and neuroprotective agent improved the situation.
... Deep brain stimulation (DBS) of different areas of the brain is the most common method used for treatment of patients with neurological problems, such as Parkinson's disease, essential tremors, etc. [Wyszkowska 2019]. Wireless magnetothermal stimulation (WMS) has recently emerged as a new method for DBS. ...
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Magnetic particle imaging (MPI) is a fast and sensitive technique for imaging of magnetic nanoparticle (MNP) concentrations. MPI directly measures and maps the particle concentration over a measured spatial position. Functional MPI (fMPI) is a specific application of MPI that aims to detect the change of cerebral blood volume (CBV) through imaging. Assuming that the concentration of MNPs in the CBV is uniform, the resultant concentration of MNPs can indicate the CBV changes. Magnetic particle spectroscopy (MPS) is basically a zero-dimensional MPI scanner which can be used to conduct spectroscopic studies and fMPI. In this letter, we suggest an MPS for fMPI with a bore size of 50 mm compatible with rat head dimensions. The system utilizes 0.015 T magnetic field at a frequency of 29.5 kHz and uses an integrated method to measure the small iron component of magnetic particles. Based on the integrated output signal, the MPS consisting of an excitation coil and a gradiometer coil with three parts—a receive coil, a cancellation coil, and a calibration coil—can detect down to 25 ng of Fe. The suggested MPS has demonstrated the achievement of sensitivity that is feasible for fMPI.
... The growing number of mobile communication devices [Mazurek et al., 2018], aparatures for medical diagnostics based on electromagnetic (EM) radiation [Gniadek-Olejniczak et al., 2018], as well as sensors for constant real-time monitoring of patients' health [Tayyab et al., 2019], raises widespread concerns about the harmful effects of electromagnetic fields (EMF) for human health [Wyszkowska et al., 2019]. These fears are particularly related to the patients with medical implants, whose number systematically increases both in general public and working environment radio-frequency (RF) field exposures [Zradzinski et al., 2019]. ...
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This paper discusses a new Implant Safety Tool, used to assess the safety of patients with metal implants exposed to radio-frequency (RF) fields. This specialist tool is discussed on the example of pectus patients with titanium bar-implant inserted during the minimally invasive Nuss procedure. The authors created a 3D realistic model of a 34-year-old male patient with a Nuss bar-implant. A numerical analysis based on the finite-difference time-domain (FDTD) method was performed for a far field source in the form of a plane wave with the frequency of 64 MHz, which corresponds to the RF exposure generated by MRI devices at 1.5 T. The obtained results allow concluding that the concave Nuss bar-implant poses no risk during environmental and occupational RF field exposures.
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Probable mechanism behind the neuronal ephaptic coupling is investigated based on the introduction of “Brain”-triggered potential excitation signal smartly with a specific very low frequency (VLF) waves as a neuronal motor toolkit. Detection of this electric motor toolkit is attributed to in-vitro precise analyses of a neural network of snail, along to the disconnected snail’s neuronal network as a control. This is achieved via rapid (real-time) electrical signals acquisition by blind patch-clamp method during micro-electrode implanting in the neurons at the gigaseal conditions by the surgery operations. This process is based on its waveform (potential excitation signal) detection by mathematical curve fitting process. The characterized waveform of this electrical signal is “Saw Tooth” that is smartly stimulated, alternatively, by the brain during triggering the action potential’s (AP’s) hyperpolarization zone at a certain time interval at the several µs levels. Triggering the neuron cells results in (1) observing a positive shift (10.0%, depending on the intensity of the triggering wave), and (2) major promotion in the electrical current from sub nano (n) to micro (µ) amper (nA, µA) levels. Direct tracing the time domain (i.e., electrical signal vs. time) and estimation of the frequency domain (diagram of electrical response vs. the applied electrical frequencies) by the “Discrete Fast Fourier Transform” algorithm approve the presence of bilateral and reversible electrical currents between axon and dendrite. This mechanism therefore opens a novel view about the neuronal motor toolkit mechanism, versus the general knowledge about the unilateral electrical current flow from axon to dendrite operations in as neural network. The reliability of this mechanism is evaluated via (1) sequential modulation and demodulation of the snail’s neuron network by a simulation electrical functions and sequentially evaluation of the neuronal current sensitivity between pA and nA (during the promotion of the signal-to-noise ratio, via averaging of 30 ± 1 (n = 15) and recycling the electrical cycles before any neuronal response); and (2) operation of the process on the differentiated stem cells. The interstice behavior is attributed to the effective role of Ca2+ channels (besides Na+ and K+ ionic pumping), during hyper/hypo calcium processes, evidenced by inductively coupled plasma as the selected analytical method. This phenomenon is also modeled during proposing quadrupole well potential levels in the neuron systems. This mechanism therefore points to the microprocessor behavior of neuron networks. Stimulation of the neuronal system based on this mechanism, not only controls the sensitivity of neuron electrical stimulation, but also would open a light window for more efficient operating the neuronal connectivity during providing interruptions by phenomena such as neurolysis as well as an efficient treatment of neuron-based disorders.
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Owing to a broad spectrum of functions performed by neuropeptides, this class of signaling molecules attracts an increasing interest. One of the key steps in the regulation of biological activity of neuropeptides is proteolytic conversion or degradation by proteinases that change or terminate biological activity of native peptides. These enzymes, in turn, are regulated by inhibitors, which play integral role in controlling many metabolic pathways. Thus, the search for selective inhibitors and detailed knowledge on the mechanisms of binding of these substances to enzymes, could be of importance for designing new pharmacological approaches. The aim of this review is to summarize the current knowledge on the inhibitors of enzymes that convert selected groups of neuropeptides, such as dynorphins, enkephalins, substance P and NPFF fragments. The importance of these substances in pathophysiological processes involved in pain and drug addiction, have been discussed. This article is part of the special issue on Neuropeptides.
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Background Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive brain stimulation technique for Alzheimer’s disease (AD). rTMS, with high- or low-frequency, is thought to enhance or inhibit the cortical activities, respectively. This meta-analysis of randomized controlled trials (RCTs) was to summarize the efficacy of the rTMS on the cognition of AD patients and to identify its potential influential factors. Methods Literature from the Pubmed, Embase, Cochrane Library and Web of Science were searched and screened to identify eligible studies. Standardized mean difference (SMD) and 95% confidence interval were used to evaluate the therapeutic effects of rTMS. Subgroup analyses were performed to investigate the influential factors. Results Ten studies with 15 trials involving 240 patients were included. Compared with sham stimulation, rTMS could significantly improve cognition in AD (SMD, 0.42; 95% CI 0.18–0.67; P = 0.0006). Subgroup analysis suggested significant cognitive enhancement in participants receiving rTMS on multiple sites rather than on single site, and in patients receiving rTMS of more than 10 sessions, but not ≤ 10 sessions. Compared with rTMS as the single therapeutic method, rTMS with concurrent cognitive training seemed to produce greater improvement. Moreover, 20 Hz rTMS, seemed to be more effective than 10 Hz or 1 Hz rTMS. Furthermore, patients with higher education, or with mild-to-moderate AD were more likely to benefit from rTMS than patients with lower education, or with severe dementia, respectively. Conclusions Based on the current evidence, rTMS was an effective therapy for cognitive impairment in AD. Large RCTs are warranted to further validate the results of our subgroup analyses.
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We have demonstrated in multiple studies that daily, long-term electromagnetic field (EMF) treatment in the ultra-high frequency range not only protects Alzheimer's disease (AD) transgenic mice from cognitive impairment, but also reverses such impairment in aged AD mice. Moreover, these beneficial cognitive effects appear to be through direct actions on the AD process. Based on a large array of pre-clinical data, we have initiated a pilot clinical trial to determine the safety and efficacy of EMF treatment to mild-moderate AD subjects. Since it is important to establish the safety of this new neuromodulatory approach, the main purpose of this review is to provide a comprehensive assessment of evidence supporting the safety of EMFs, particularly through transcranial electromagnetic treatment (TEMT). In addition to our own pre-clinical studies, a rich variety of both animal and cell culture studies performed by others have underscored the anticipated safety of TEMT in clinical AD trials. Moreover, numerous clinical studies have determined that short- or long-term human exposure to EMFs similar to those to be provided clinically by TEMT do not have deleterious effects on general health, cognitive function, or a variety of physiologic measures-to the contrary, beneficial effects on brain function/activity have been reported. Importantly, such EMF exposure has not been shown to increase the risk of any type of cancer in human epidemiologic studies, as well as animal and cell culture studies. In view of all the above, clinical trials of safety/efficacy with TEMT to AD subjects are clearly warranted and now in progress.
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The defining features of Alzheimer disease (AD) include conspicuous changes in both brain histology and behavior. The AD brain is characterized microscopically by the combined presence of 2 classes of abnormal structures, extracellular amyloid plaques and intraneuronal neurofibrillary tangles, both of which comprise highly insoluble, densely packed filaments. The soluble building blocks of these structures are amyloid-β (Aβ) peptides for plaques and tau for tangles. Amyloid-β peptides are proteolytic fragments of the transmembrane amyloid precursor protein, whereas tau is a brain-specific, axon-enriched microtubule-associated protein. The behavioral symptoms of AD correlate with the accumulation of plaques and tangles, and they are a direct consequence of the damage and destruction of synapses that mediate memory and cognition. Synapse loss can be caused by the failure of live neurons to maintain functional axons and dendrites or by neuron death. During the past dozen years, a steadily accumulating body of evidence has indicated that soluble forms of Aβ and tau work together, independently of their accumulation into plaques and tangles, to drive healthy neurons into the diseased state and that hallmark toxic properties of Aβ require tau. For instance, acute neuron death, delayed neuron death following ectopic cell cycle reentry, and synaptic dysfunction are triggered by soluble, extracellular Aβ species and depend on soluble, cytoplasmic tau. Therefore, Aβ is upstream of tau in AD pathogenesis and triggers the conversion of tau from a normal to a toxic state, but there is also evidence that toxic tau enhances Aβ toxicity via a feedback loop. Because soluble toxic aggregates of both Aβ and tau can self-propagate and spread throughout the brain by prionlike mechanisms, successful therapeutic intervention for AD would benefit from detecting these species before plaques, tangles, and cognitive impairment become evident and from interfering with the destructive biochemical pathways that they initiate.
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To estimate the relationship between exposure to extremely low-frequency electromagnetic fields (ELF-EMF) and the risk of amyotrophic lateral sclerosis (ALS) by a meta-analysis. Through searching PubMed databases (or manual searching) up to April 2012 using the following keywords: "occupational exposure", "electromagnetic fields" and "amyotrophic lateral sclerosis" or "motor neuron disease", seventeen studies were identified as eligible for this meta-analysis. The associations between ELF-EMF exposure and the ALS risk were estimated based on study design (case-control or cohort study), and ELF-EMF exposure level assessment (job title or job-exposure matrix). The heterogeneity across the studies was tested, as was publication bias. Occupational exposure to ELF-EMF was significantly associated with increased risk of ALS in pooled studies (RR = 1.29, 95%CI = 1.02-1.62), and case-control studies (OR = 1.39, 95%CI = 1.05-1.84), but not cohort studies (RR = 1.16, 95% CI = 0.80-1.69). In sub-analyses, similar significant associations were found when the exposure level was defined by the job title, but not the job-exposure matrix. In addition, significant associations between occupational exposure to ELF-EMF and increased risk of ALS were found in studies of subjects who were clinically diagnosed but not those based on the death certificate. Moderate heterogeneity was observed in all analyses. Our data suggest a slight but significant ALS risk increase among those with job titles related to relatively high levels of ELF-EMF exposure. Since the magnitude of estimated RR was relatively small, we cannot deny the possibility of potential biases at work. Electrical shocks or other unidentified variables associated with electrical occupations, rather than magnetic-field exposure, may be responsible for the observed associations with ALS.
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Purpose: Epidemiological data suggest that there is a link between exposure to extremely low-frequency magnetic fields (ELF-MFs), immune response and the occurrence of neurodegenerative diseases. The exact nature of this phenomenon remains speculative and requires detailed laboratory investigation. In the present study we evaluate changes in plasma concentration of pro-inflammatory and regulatory cytokines as well as alternations of the haematological parameters in rats exposed to an ELF-MF. Materials and Methods: Male Wistar rats were repeatedly exposed for either 1h/day for 7 days, or continuously for 24h, to a sinusoidal ELF-MF (50 Hz, 7 mT). Control groups were sham exposed for either 1h/day for 7 days, or continuously for 24h, respectively. The levels of cytokines: interleukin (IL)-1β, IL-2, IL-6 and IL-10 in plasma obtained from blood samples were determined using enzyme-linked immunosorbent assay (ELISA). Changes in blood parameters were determined using an automatic haematology analyser in whole blood samples immediately after collection. Results: We found that a single continuous (lasting 24h) exposure provoked a significant increase of the plasma IL-1β, IL-6 and IL-2 levels, and caused an elevation in blood parameters, such as white blood cells, lymphocytes, haemoglobin and haematocrit levels. In contrast, however, repetitive exposure of rats to an ELF-MF for 1h/day for 7 days did not lead to any changes in plasma levels of cytokines and haematological counts. Conclusions: Based on these data we conclude that exposure duration (dose-response) plays a significant role for the immune response, specifically at the cellular level. While single 24h-lasting exposure provoked changes that indicate an immune alarm stimulation, under the conditions which are typical for therapeutic use of ELF-MFs (repeated short daily exposure) the immune potentially harmful response has not been observed.
Conference Paper
Unambiguous design of each coil, applied in Transcranial Magnetic Stimulation (TMS) procedure, involves assigning it a set of parameters. The use of just a few or several, real-valued parameters for this purpose is convenient, and renders the optimization procedure less complicated. Hence, using parametric curves is an appropriate method. Several types of coils used in TMS procedure are presented. Each of them is characterized by a set of parameters that, coupled with five others that describe the shift and rotation of the coil in space, allow a clear characterization of the device, as well as its position relative to the patient's body. This approach is related to the basic aspects of optimization in biomedical engineering.
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The paper deals with the problems connected with the electromagnetic therapy used in orthopaedic diseases. The electromagnetic background of the treatment is briefly discussed as well as the particular techniques are grouped. The effectiveness of the techniques is quoted and the method of magnetotherapy is showed as the most useful technique. As eddy currents play the main role in magnetotherapy they are numerically simulated for two arrangements. The discussion on the technical parameters of the therapy as well as on the hazardous aspect is carried out.
Article
The results of the research which has been done for the last few years indicate the lack of unambiguous efficiency of transcranial magnetic stimulation (TMS) in the therapeutic area. However, it is effective in the area of diagnosis. In both areas we need to know the electromagnetic field distribution which is determined by the shape of stimulating coil. In the paper we present the analysis of electromagnetic field in the case of the application of a butterfly coil. © 2014, Wydawnictwo SIGMA - N O T Sp. z o.o. All rights reserved.
Article
Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. Brain injuries are highly heterogeneous, and can also trigger other neurological complications, including epilepsy, depression and dementia. The initial injury often leads to the development of secondary sequelae; cellular hyper-excitability, vasogenic and cytotoxic oedema, hypoxia-ischemia, oxidative stress and inflammation, all of which influence expansion of the primary lesion. It is widely known that inflammatory events in the brain following TBI contribute to the widespread cell death and chronic tissue degeneration. Neuro-inflammation is a multi-faceted response involving a number of cell types, both within the central nervous system (CNS) and in the peripheral circulation. Astrocytes and microglia, cells of the CNS, are considered key players in initiating an inflammatory response after injury. These cells are capable of secreting various cytokines, chemokines and growth factors, and following injury to the CNS, undergo changes in morphology. Ultimately, these changes can influence the local microenvironment and thus determine the extent of damage and subsequent repair. This review will focus on the roles of microglia and astrocytes following TBI, highlighting some of the key processes, pathways and mediators involved in this response. Additionally, both the beneficial and detrimental aspects of these cellular responses will be examined, using evidence from animal models and human post-mortem TBI studies. This article is protected by copyright. All rights reserved.