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PEMF For Alzheimer’s Disease

Disclaimer: Please note that these pages are for general information purposes only. The opinions and information have not been evaluated by the FDA.  They should not be considered complete in terms of the physical conditions discussed, or construed as healthcare advice.

Alzheimer’s disease (AD) is a progressive brain disorder that slowly destroys memory, thinking skills and, eventually, the ability to carry out the simplest tasks.  Alzheimer’s disease is thought to be caused by the abnormal build-up of proteins in and around brain cells.  One of the proteins involved is called amyloid, deposits of which form plaques around brain cells.  The other protein is called tau, deposits of which form tangles within brain cells. [1] In Alzheimer’s disease, as neurons (brain cells) are injured and die throughout the brain, connections between networks of neurons may break down, and many brain regions begin to shrink.  There is currently no effective treatment against Alzheimer’s disease, and its pathogenesis (how it occurs) remains unclear. [2] A lot of studies on Alzheimer’s disease have highlighted the possible involvement of genetic [3], immunological [4], and environmental causes. [5] Oxidative stress, disruption of calcium homeostasis, hormonal factors, inflammation, and vascular and cell cycle dysregulations have been associated with the disease. [6] While there is no cure for Alzheimer’s disease or a way to stop or slow its progression, there are drug and non-drug options that may help treat symptoms.  Understanding available options can help individuals living with the disease and their caregivers to cope with symptoms and improve quality of life.

A pioneering field of research in Alzheimer’s disease is brain stimulation via Electromagnetic fields (EMF), which seems to modulate or change the neurophysiological (brain functioning) activity of pathological (dysfunctional) circuits and produce clinical benefits in Alzheimer’s disease patients. [7] EMF induced cortical (brain tissue) changes have resulted in enhanced neural plasticity (function and adaption of brain cells).  Enhancement of the brain cortical excitability (brain activity) might induce a specific potentiation-like (increase in activity) phenomenon, which would enable synaptic (brain nerve connection) plasticity and promote recovery or improvement of a degraded (lost or changed) function.  Given these premises, there is currently a growing interest in applying EMFs as a therapeutic approach in psychiatric and neurological disorders. [8,9]

For instance, it has been found that EMF stimulation of the brain through pulsed electromagnetic fields (PEMF) can establish the reactivation of cognitive (thinking) processes in Alzheimer’s disease; protecting against impairment and improving memory and demonstrated the reduction of amyloid plaques in transgenic mice models. [10] Moreover, EMF, which interacts in a noninvasive way with the nervous system, could be clinically used to re-establish cognitive performance in stroke patients [11,9] and in patients suffering from neurodegenerative diseases. [12,13]

EMFs have shown to modulate the functions of the cytoskeleton (cell skeleton) and to promote the neuronal differentiation (brain cells defining their function) and the neurogenesis (new brain cell growth) in the hippocampus in vivo through the upregulation (increasing) of the Cav-1 channel, [14, 15, 16, 17] β-III-tubulin, MAP2, [18] and the brain-derived neurotrophic factor (BDNF). [19] When these channels, proteins and neurotrophic factors work better, we see improvement of the brain cell function, and the stimulation of both cell repair and new cell growth.  BDNF is widely expressed in the brain and contributes to a variety of neuronal processes affecting the neurodevelopment, the survival, and the maintenance of the homeostasis (balance) of the nervous system in the elderly. [16] In the adult brain, BDNF plays a key role in the modulation of the synaptic plasticity and it is essential for the regulation of memory. For these reasons, data supports the hypothesis that EMF could improve the brain neuroplasticity also through the modulation of the expression of neurotrophic factors. [20]

Of interest, it has been demonstrated, in vitro, that both low- and high-frequency EMFs can also modulate gene expression by acting on both transcriptional (copying DNA or RNA) and posttranscriptional regulatory mechanisms. [21, 22, 23] Within this context, in both physiological (healthy) and pathological (unhealthy) conditions, posttranscriptional mechanisms are key determinants of the gene expression modulation, since genes control the rapid adaptation of protein levels to changing environmental conditions, they can differently influence the cell fate. These mechanisms include the implication of a class of small noncoding RNA molecules, called miRNAs (microRNA), able to regulate the gene expression mainly by base pairing to the 3′-UTR of specific target mRNAs (messenger RNA). [24]

Which means the miRNA links or bonds to a specific site (the 3’-UTR location) on the target mRNA, which then controls gene expression.  Considering that miRNAs are predicted to regulate up to 90% of human genes [25], their physiological activity is critical for the maintenance of healthy conditions and their aberrant expression is associated with the pathological features of many diseases. [24, 25, 26] PEMF exposure modulates the expression of miRNAs that regulate the brain signaling, confirming the capacity of the electromagnetic field to stimulate both tissue regeneration and brain signaling.  The study confirmed the capacity of PEMF to influence various networks of physiological functions that are dysregulated (loss of regulation of function) in Alzheimer’s disease.  Among the effects observed, a quantitative reduction of β-secretase, following PEMF exposure, could confirm a protective effect of the electromagnetic field whose action would counteract the formation of Amyloid. [27]

These results suggest that EMFs if properly applied, may be useful for the treatment of patients with Alzheimer’s disease, as suggested by the results of pilot experiments with EMFs, which were reported to produce clinical benefits. [7] However, it is of course necessary to take account of the complex network of epigenetic signals, not yet completely known that lead to the development and progression of Alzheimer’s disease.  Further studies are needed in order to investigate the effects of EMF and develop the conditions useful for a therapeutic protocol.

Dr. Amanda Myers, MD, MSPH

MagnaWave Medical Director

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Amyloid plaques are aggregates of misfolded proteins that form in the spaces between nerve cells. These abnormally configured proteins are thought to play a central role in Alzheimer’s disease. The amyloid plaques first develop in the areas of the brain concerned with memory and other cognitive functions. Back

Post-transcriptional regulation is the control of gene expression at the RNA level, therefore between the transcription and the translation of the gene. It contributes substantially to gene expression regulation across human tissues. Back

Ribonucleic acid (RNA) is a linear molecule composed of four types of smaller molecules called ribonucleotide bases: adenine (A), cytosine (C), guanine (G), and uracil (U). Back

Aberrant phenotype is a phenomenon of abnormal expression or loss of expression of cell specific lineage marker not associated with specific cell type. Aberrant phenotype expression due to genetic defects may be associated with unfavorable outcome. It can be used to determine minimal residual disease status. Back

Amyloid refers to the abnormal fibrous, extracellular, proteinaceous deposits found in organs and tissues. Amyloid is insoluble and is structurally dominated by β-sheet structure. Back

Epigenetic signals are responsible for the establishment, maintenance, and reversal of metastable transcriptional states that are fundamental for the cell’s ability to “remember” past events, such as changes in the external environment or developmental cues. Back

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